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Acute Pyelonephritis
Updated: Jun 14, 2019
Author: Tibor Fulop, MD, PhD, FACP, FASN; Chief Editor: Vecihi Batuman, MD, FASN

Overview

Practice Essentials
Acute pyelonephritis is a bacterial infection of the renal parenchyma that can be organ- and/or life-threatening and that often
leads to renal scarring. The bacteria in these cases have usually ascended from the lower urinary tract, but may also reach the
kidney via the bloodstream. Timely diagnosis and management of acute pyelonephritis has a significant impact on patient
outcomes.[1, 2] See the image below.

Multiple abscesses, upper pole of left kidney.

Signs and symptoms


The classic presentation in patients with acute pyelonephritis is as follows:

Fever - This is not always present, but when it is, it is not unusual for the temperature to exceed 103°F (39.4°C)

Costovertebral angle pain - Pain may be mild, moderate, or severe; flank or costovertebral angle tenderness is most
commonly unilateral over the involved kidney, although bilateral discomfort may be present

Nausea and/or vomiting - These vary in frequency and intensity, from absent to severe; anorexia is common in patients
with acute pyelonephritis

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Gross hematuria (hemorrhagic cystitis), unusual in males with pyelonephritis, occurs in 30-40% of females, most often young
women, with the disorder.

Symptoms usually develop over hours or over the course of a day but may not occur at the same time. If the patient is male,
elderly, or a child or has had symptoms for more than 7 days, the infection should be considered complicated until proven
otherwise.

The classic manifestations of acute pyelonephritis observed in adults are often absent in children, particularly neonates and
infants. In children aged 2 years or younger, the most common signs and symptoms of urinary tract infection (UTI) are as
follows:

Failure to thrive
Feeding difficulty
Fever
Vomiting

Elderly patients may present with typical manifestations of pyelonephritis, or they may experience the following:

Fever
Mental status change
Decompensation in another organ system
Generalized deterioration

See Presentation for more detail.

Diagnosis
In the outpatient setting, pyelonephritis is usually suggested by a patient’s history and physical examination and supported by
urinalysis results. Urine specimens can be collected through the following methods:

Clean catch
Urethral catheterization
Suprapubic needle aspiration

Urinalysis can include the following:

Dipstick leukocyte esterase test (LET) - Helps to screen for pyuria


Nitrite production test (NPT) - To screen for bacteriuria
Examination for hematuria (gross and microscopic) and proteinuria

Urine culture is indicated in any patient with pyelonephritis, whether treated in an inpatient or outpatient setting, because of the
possibility of antibiotic resistance.

Imaging studies that may be used in assessing acute pyelonephritis include the following:

Computed tomography (CT) scanning - To identify alterations in renal parenchymal perfusion; alterations in contrast
excretion, perinephric fluid, and nonrenal disease; gas-forming infections; hemorrhage; inflammatory masses; and
obstruction

Magnetic resonance imaging (MRI) – To detect renal infection or masses and urinary obstruction, as well as to evaluate
renal vasculature

Ultrasonography - To screen for urinary obstruction in children admitted for febrile illnesses and to examine patients for
renal abscesses, acute focal bacterial nephritis, and stones (in xanthogranulomatous pyelonephritis)

Scintigraphy - To detect focal renal abnormalities

CT and MR urography - Used in the evaluation of hematuria

See Workup for more detail.

Management

Antibiotic therapy is essential in the treatment of acute pyelonephritis and prevents progression of the infection. Urine culture
and sensitivity testing should always be performed, and empirical therapy should be tailored to the infecting uropathogen.[3]

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Patients presenting with complicated pyelonephritis should be managed as inpatients and treated empirically with broad-
spectrum parenteral antibiotics.

Outpatient care

Outpatient treatment is appropriate for patients who have an uncomplicated infection that does not warrant hospitalization.
Treatment can be with a single dose of a parenteral antibiotic followed by oral therapy, provided that the patient is monitored
within the first 48 hours.

Inpatient care

Inpatient care includes the following:

Supportive care
Monitoring of urine and blood culture results
Monitoring of comorbid conditions for deterioration
Maintenance of hydration status with IV fluids until hydration can be maintained with oral intake
IV antibiotics until defervescence and significant symptomatic improvement occur; convert to an oral regimen tailored to
urine or blood culture results

Surgery

In addition to antibiotics, surgery may be necessary to treat the following manifestations of acute pyelonephritis:

Renal cortical abscess (renal carbuncle): Surgical drainage (if patients do not respond to antibiotic therapy); other
surgical options are enucleation of the carbuncle and nephrectomy

Renal corticomedullary abscess: Incision and drainage, nephrectomy

Perinephric abscess: Drainage, nephrectomy

Calculi-related urinary tract infection (UTI): Extracorporeal shockwave lithotripsy (ESWL) or endoscopic, percutaneous,
or open surgery

Renal papillary necrosis: CT scan ̶ guided drainage or surgical drainage with debridement

Xanthogranulomatous pyelonephritis: Nephrectomy

See Treatment and Medication for more detail.

Background
Acute pyelonephritis is a potentially organ- and/or life-threatening infection that characteristically causes scarring of the kidney.
[4] An episode of acute pyelonephritis may lead to significant renal damage; acute kidney injury; abscess formation (eg, nephric,
perinephric); sepsis; or sepsis syndrome, septic shock, and multiorgan system failure.

A population-based study of acute pyelonephritis in the United States found overall annual rates of 15–17 cases per 10,000
females and 3–4 cases per 10,000 males.[5]

Diagnosing and managing acute pyelonephritis is not always straightforward. Wide variation exists in the clinical presentation,
severity, options, and disposition of the disease.

Patients in the age range of 5-65 years typically present with lower urinary tract infection (UTI) symptoms (eg, dysuria,
frequency, urgency, gross hematuria, suprapubic pain) and classic upper UTI symptoms (eg, flank pain, back pain), with or
without systemic signs and symptoms (eg, fever, chills, abdominal pain, nausea, vomiting, costovertebral angle tenderness) and
with or without leukocytosis. However, acute pyelonephritis can present as nonspecific symptoms.

A number of studies using immunochemical markers have shown that many women who initially present with lower urinary tract
symptoms actually have pyelonephritis. Their pyelonephritis is often identified when short-course therapy for uncomplicated
cystitis fails.

With patients at the extremes of age, the presentation may be so atypical that pyelonephritis is not in the differential diagnosis.
Infants may present with feeding difficulty or fever, and the elderly may have mental status change or fever.

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Acute pyelonephritis is complex, and there is no consistent set of signs and symptoms that is both sensitive and specific for the
diagnosis. Therefore, clinicians must maintain a high index of suspicion.

In contrast to the plethora of data available for the treatment of cystitis, less substantial data are available regarding the
appropriate antibiotic choice or duration of therapy for acute pyelonephritis. An additional cause for concern is the growing
resistance of uropathogens to standard agents. Nevertheless, useful recommendations can be made.

The current emphasis on cost-effectiveness and the advent of newer antibiotics have led clinicians to reevaluate the benefit of
hospitalization in patients with acute pyelonephritis. Most cases of uncomplicated pyelonephritis in young women can be
managed successfully on an outpatient basis. However, outpatient management of acute pyelonephritis requires close follow-up
care. The first follow-up visit should occur in 1-2 days, depending on the clinician's estimation of the severity of the infection. Any
deterioration or unsatisfactory improvement warrants admission for intravenous antibiotics and evaluation for any complications.
(See Treatment.)

Complicated pyelonephritis results from structural and functional abnormalities, urologic manipulations, or underlying disease; it
includes pyelonephritis in men and in the elderly. Any patient with complicated pyelonephritis should be referred, if possible, to a
physician trained in the management of these cases (eg, a nephrologist, urologist, or infectious disease specialist). The patient
will require ongoing management, including repeat cultures, metabolic studies, and appropriate imaging studies.

Pathophysiology
Acute pyelonephritis results from bacterial invasion of the renal parenchyma. Bacteria usually reach the kidney by ascending
from the lower urinary tract.[6] In all age groups, episodes of bacteriuria occur commonly, but most are asymptomatic and do not
lead to infection. The development of infection is influenced by bacterial factors and host factors.[7]

Bacteria may also reach the kidney via the bloodstream. Hematogenous sources of gram-positive organisms, such as
Staphylococcus, are intravenous drug abuse and endocarditis. Experimental evidence suggests that hematogenous spread of
gram-negative organisms to the kidney is less likely unless an underlying problem exists, such as an obstruction. Little or no
evidence supports lymphatic spread of uropathogens to the kidney.

Most bacterial data are derived from research with Escherichia coli, which accounts for 70-90% of uncomplicated UTIs and 21-
54% of complicated UTIs (ie, UTIs that are secondary to anatomic or functional abnormalities that impair urinary tract drainage;
are associated with metabolic disorders; or involve unusual pathogens). A subset of E coli, the uropathogenic E coli (UPEC),
also termed extraintestinal pathogenic E coli (ExPEC), accounts for most clinical isolates from UTIs.

UPEC derives commonly from the phylogenetic groups B2 and D, which express distinctive O, K, and H antigens. UPEC genes
encode several postulated virulence factors (VFs), including adhesins, siderophores, protectins, and toxins, as well as having
the metabolic advantage of synthesizing essential substances.

Virulence factors

Adhesins have specific regions that attach to cell receptor epitopes in a lock-and-key fashion. Mannose-sensitive adhesins
(usually type 1 fimbriae) are present on essentially all E coli. They contribute to colonization (eg, bladder, gut, mouth, vagina)
and possibly pathogenesis of infection; however, they also attach to polymorphonuclear neutrophils (PMNs), leading to bacterial
clearance.

Mannose-resistant adhesins permit the bacteria to attach to epithelial cells, thereby resisting the cleansing action of urine flow
and bladder emptying. They also allow the bacteria to remain in close proximity to the epithelial cell, enhancing the activity of
other VFs.

The P fimbriae family of adhesins is epidemiologically associated with prostatitis, pyelonephritis (70-90% of strains), and sepsis.
This family of adhesins is associated with less than 20% of asymptomatic bacteriuria (ABU) strains. The AFA/Dr family is
associated with diarrhea, UTI, and particularly pyelonephritis in pregnancy. The S/F1C family is associated with neonatal
meningitis and UTI.

Siderophores are involved in iron uptake, an essential element for bacteria, and possibly adhesion. Protectins and their
contributions to virulence include the following:

Lipopolysaccharide (LPS) coatings: resist phagocytosis


Tra T and Iss: resist action of complement
Omp T: cleave host defense proteins (eg, immunoglobulins)

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Toxins, which affect various host cell functions, include the following:

Alpha-hemolysin
Cytotoxic necrotizing factor–1
Cytolethal distending toxin
Secreted autotransporter toxin

No single VF is sufficient or necessary to promote pathogenesis. Apparently, multiple VFs are necessary to ensure
pathogenesis, although adhesins play an important role.

Asymptomatic bacteriuria strains

Bacterial strains that produce ABU may in some instances provide a measure of protection against symptomatic infections from
UPEC and other organisms. On the other hand, ABU may also cause increased morbidity and mortality. Once bacteriuria is
established, these strains appear to stop producing adhesins, allowing them to survive and persist without producing an
inflammatory reaction.

Pathogens

As noted above, UPEC account for most uncomplicated pyelonephritis cases and a significant portion of complicated
pyelonephritis cases. The following microorganisms are also commonly isolated:

Staphylococcus saprophyticus
Klebsiella pneumoniae
Proteus mirabilis
Enterococci
S aureus
Pseudomonas aeruginosa
Enterobacter species

This is the same spectrum of organisms cultured in cystitis. In 10-15% of symptomatic cystitis cases, cultures using routine
methods remain negative, although the symptoms typically respond to antibiotic therapy. In some cases, cultures using selective
media have grown Gardnerella vaginalis, Mycoplasma hominis, and Ureaplasma urealyticum. These data cannot be extended
to acute pyelonephritis, but they do illustrate the difficulties in isolating the causative organism.

Epithelial attachment and inflammatory response

Evidence suggests that the pathogenesis of pyelonephritis takes a 2-step path. First, UPEC attaches to the epithelium and
triggers an inflammatory response involving at least 2 receptors, glycosphingolipid (GSL) and Toll-like receptor 4 (TLR4). In the
mouse model, GSL is the primary receptor and TLR4 is recruited and is an important receptor for the release of chemokines.
When TLR4 is genetically absent, an asymptomatic carrier state develops in the infected mice.

Second, as a result of the inflammatory response, chemokines (eg, interleukin-8 [IL-8], which is chemotactic for PMNs) are
released and attach to the neutrophil-activating chemokine receptor 1 (CXCR1), allowing PMNs to cross the epithelial barrier
into the urine. In children prone to pyelonephritis, for example, CXCR1 expression has been shown to be significantly lower than
in control subjects.

Several other host factors militate against symptomatic UTI. Phagocytosis of bacteria in urine is maximized at pH 6.5-7.5 and
osmolality of 485 mOsm; values deviating from these ranges lead to significantly reduced or absent phagocytosis. Other
important factors are the flushing action of urine flow in the ureter and bladder, the inhibition of attachment of type 1 fimbriae E
coli to uroepithelial cells by tubular cell–secreted Tamm-Horsfall protein, and the inhibition of attachment by some surface
mucopolysaccharides on the uroepithelial cells.

Complicated infection

Complicated UTI is an infection of the urinary tract in which the efficacy of antibiotics is reduced because of the presence of one
or more of the following:

Structural abnormalities of the urinary tract


Functional abnormalities of the urinary tract
Metabolic abnormalities predisposing to UTIs
Unusual pathogens
Recent antibiotic use
Recent urinary tract instrumentation

For more information on this topic, see Pathophysiology of Complicated Urinary Tract Infections.
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Obstruction

Obstruction is the most important factor. It negates the flushing effect of urine flow; allows urine to pool (urinary stasis), providing
bacteria a medium in which to multiply; and changes intrarenal blood flow, affecting neutrophil delivery. Obstruction may be
extrinsic or intrinsic. Extrinsic obstruction occurs with chronic constipation (particularly in children), prostatic swelling/mass (eg,
hypertrophy, infection, cancer), and retroperitoneal mass.

Intrinsic obstruction occurs with bladder outlet obstruction, cystocele, fungus ball, papillary necrosis, stricture, and urinary
stones. With increasing size of stone, the probability of stone passage decreases while the probability of obstruction increases.
Nonetheless, stones as small as 2 mm have resulted in obstruction, while 8-mm stones have occasionally passed
spontaneously.

Infectious stones, urease stones, or triple-phosphate stones composed of magnesium ammonium phosphate or struvite and
apatite account for 10-15% of all urinary stones. They develop secondary to the action of urea-splitting organisms and can grow
rapidly and branch out (ie, staghorn calculi).

If left untreated, staghorn calculi will destroy the kidney and may cause the death of the patient. Complications include azotemia,
hydropyonephrosis, perinephric abscess, pyelonephritis (severe or end-stage), sepsis, and xanthogranulomatous pyelonephritis.

Incomplete bladder emptying may be related to medication (eg, anticholinergics). The spermicide nonoxynol-9 inhibits the
growth of lactobacilli. Lactobacilli produce hydrogen peroxide, which protects the vaginal ecosystem against pathogens.
Frequent sexual intercourse causes local mechanical trauma to the urethra in both partners.

Atrophic vaginal mucosa in postmenopausal women predisposes to the colonization of urinary tract pathogens and UTIs
because of the higher pH (5.5 vs 3.8) and the absence of lactobacilli. Bacterial prostatitis (acute or chronic) produces
bacteriuria, whereas nonbacterial prostatitis and pelviperineal pain syndrome (prostadynia) do not.

Unusual organisms include Mycoplasma, Pseudomonas, and urea-splitting organisms. Pseudomonas aeruginosa has several
mechanisms that promote adherence, including alginate, other membrane proteins, pili, and surface-associated exoenzyme S.

Urea-splitting organisms produce urease, which hydrolyzes urea, yielding ammonia, bicarbonate, and carbonate; this leads to a
more alkaline urine and allows crystal formation (staghorn calculus) from the supersaturation of carbonate apatite and struvite.
Staghorn calculi continue to grow in size, leading to infection, obstruction, or both.

Complications of obstruction with superimposed infection include hydronephrosis, pyonephrosis, urosepsis, and
xanthogranulomatous pyelonephritis. Additionally, the pathogens can sequester in the struvite stones, protected from the host’s
immune system. Proteus species are the most common urea-splitting organisms. E coli, Klebsiella, Pseudomonas, and
Staphylococcus can also produce urease, however, and are sometimes involved in staghorn calculus formation.

Pregnancy

Pregnancy produces hormonal and mechanical changes that predispose the woman to upper urinary traction infections.
Hydroureter of pregnancy, secondary to both hormonal and mechanical factors, manifests as dilatation of the renal pelvis and
ureters (greater on the left than on the right), with the ureters containing up to 200 mL of urine. Progesterone decreases ureteral
peristalsis and increases bladder capacity. The enlarging uterus displaces the bladder, contributing to urinary stasis.

Diabetes

Diabetes mellitus produces autonomic bladder neuropathy, glucosuria, leukocyte dysfunction, microangiopathy, and
nephrosclerosis; additionally, it leads to recurrent bladder instrumentation secondary to the neuropathy. Complicated UTIs in
patients who have diabetes mellitus include the following:

Renal and perirenal abscess


Emphysematous pyelonephritis
Emphysematous cystitis
Fungal infections
Xanthogranulomatous pyelonephritis
Papillary necrosis

Etiology

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Uropathogens that cause the majority of acute pyelonephritis cases and the frequency with which they are cultured in
uncomplicated versus complicated cases, are listed in Table 1. Unusual pathogens include mycobacteria, yeasts and fungi, and
opportunistic pathogens such as Corynebacterium urealyticum.

Table 1. Bacterial Etiology of Urinary Tract Infections (Open Table in a new window)

Bacteria % Uncomplicated % Complicated

Gram negative

Escherichia coli 70-95 21-54

Proteus mirabilis 1-2 1-10

Klebsiella spp 1-2 2-17

Citrobacter spp <1 5

Enterobacter spp <1 2-10

Pseudomonas aeruginosa <1 2-19

Other <1 6-20

Gram positive

Coagulase-negative staphylococci 5-10* 1-4

Enterococci 1-2 1-23

Group B streptococci <1 1-4

Staphylococcus aureus <1 1-23

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Other <1 2

Adapted from Hooton TM. The current management strategies for community-acquired urinary tract infection. Infect Dis
Clin North Am. Jun 2003;17(2):303-32. [Medline].

* S saprophyticus

Epidemiology
Epidemiologic data on the incidence of pyelonephritis are limited. A population-based study of acute pyelonephritis in the United
States found overall annual rates of 15-17 cases per 10,000 females and 3-4 cases per 10,000 males.[5] In women aged 18−49 
years, the estimated incidence is 28 cases per 10,000.[40] At least 250,000 cases of pyelonephritis are diagnosed annually in
the United States. The cost of treating acute pyelonephritis has been estimated to be $2.14 billion per year.[5]

Acute pyelonephritis develops in 20-30% of pregnant women with untreated asymptomatic bacteriuria (ABU) (2-9.5%), most
often during the late second and early third trimesters. The incidence of pyelonephritis in infants and children is difficult to
ascertain because of the infrequency of typical symptoms. Up to 25% of children with UTI and no signs or symptoms of
pyelonephritis do have bacteria demonstrable in the upper urinary tract.

No racial predilection of pyelonephritis has been demonstrated. Pyelonephritis is significantly more common in females than in
males, although this difference narrows considerably with increasing age, especially in patients aged 65 years and older. In
females, pyelonephritis shows a trimodal distribution, with an elevated incidence in girls aged 0-4 years, a peak in women 15-35
years of age, and a gradual increase after age 50 years to another peak at 80 years of age.[5]

In males, the age distribution of pyelonephritis is bimodal. Males also demonstrate a peak incidence of pyelonephritis at 0-4
years of age. Rates gradually increase after 35 years of age and peak at 85 years of age.[5]

Acute pyelonephritis shows a seasonal variation. In Washington state, cases occurred most frequently during the months of July
and August among females and during August and September in the male population.[5]

Prognosis
Timely diagnosis and management of acute pyelonephritis has a significant impact on the outcome. Any patient with acute
pyelonephritis who deteriorates suddenly or does not respond to conventional therapy may have a complication, resistant
organism, or unrecognized comorbidity.

Pyelonephritis causes considerable morbidity. Data can be extrapolated from the morbidity data for acute lower urinary tract
infections: specifically, acute cystitis in women produces approximately 6.1 days with symptoms, 2.4 days of restricted activity,
1.2 days that the patient is unable to work or attend class, and 0.4 days bedridden. In women aged 18−49 years, 7% of
pyelonephritis cases require hospital admission.[40]

For patients with pyelonephritis who have an organ-threatening infection, the follow-up examination is important to be sure that
the patient is progressing satisfactorily and that recovery is complete. Failure to diagnose these complications in a timely fashion
could predispose the patient to a poor outcome. Pregnant patients with pyelonephritis are at significant risk for premature labor.

Kofteridis et al found that acute pyelonephritis is linked to bacteremia, longer hospital stays, and higher mortality in patients with
diabetes mellitus.[8] In a retrospective study of 206 elderly patients, 88 of whom had diabetes, bacteremia occurred in 30.7% of
patients with diabetes but in only 11% of the control patients. Moreover, compared with the control patients, patients with
diabetes had longer-lasting fevers (median, 4.5 vs 2.5 days), longer hospital stays (median, 10 vs 7 days), and higher mortality
(12.5% vs 2.5%).
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Mortality is higher in patients older than 65 years; it is also higher with septic shock, bedridden status, and immunosuppression.
In men, mortality is also increased with use of antibiotics during the previous month. Morbidity (prolonged hospital stay) in both
men and women is increased with a change in initial treatment, diabetes mellitus, and long-term indwelling catheter.

Uncomplicated pyelonephritis

In healthy, nonpregnant women with uncomplicated disease, the prognosis is excellent for full recovery and minimal damage to
the kidney. In healthy men without any known complicating conditions, the prognosis is good for full recovery; however, urologic
evaluation is recommended to rule out an underlying complicating condition. In infants and children, the prognosis is good.
Importantly, children should undergo a urologic evaluation after the first episode to rule out structural abnormalities.

Uncomplicated pyelonephritis is not a fatal disease in the antibiotic era. Pyelonephritis becomes a potentially fatal disease when
secondary conditions develop, such as emphysematous pyelonephritis (20-80% mortality rate), perinephric abscess (20-50%
mortality rate), or one of the sepsis syndromes (>25% overall mortality rate).

Emphysematous pyelonephritis

In emphysematous pyelonephritis, the mortality rate is 60% in cases in which the gas is localized to the renal parenchyma,
regardless of treatment. The mortality is 80% if the gas has spread in the perinephric space and the patient is treated with
antibiotics alone. In emphysematous pyelitis, the mortality rate is 20%.

Sepsis

The genitourinary system is the source of severe sepsis in 9.1% of all cases annually. The mortality for these GU-related cases
is 16.1%. Overall mortality from severe sepsis significantly increases with chronic renal disease (36.7%), acute renal dysfunction
(38.2%), and age older than 64 years (25-42% with progressively increasing age to older than 85 years). In the age range of 0-4
years, the mortality is 5%; for ages 5-50 years, it is less than 3%.

Acute kidney injury

Rarely, acute pyelonephritis can cause acute kidney injury (AKI) in children, healthy adults, and pregnant women. When this
occurs, characteristically, recovery proceeds more slowly than with AKI from other causes. In most instances, other factors are
thought to contribute to the AKI (eg, medications, hypovolemia, obstruction, sepsis). In a retrospective review of 403 adult
patients hospitalized for acute pyelonephritis, multivariate analysis showed that age over 65, complicated or bilateral
pyelonephritis, and initial shock were independent risk factors for the occurrence of AKI.[37]

Renal scarring

In children, renal scarring can be detected in 6-15% after a febrile UTI. Of these patients, almost all males and some females
have demonstrable renal scarring and a globally small kidney with smooth renal outlines in infancy, usually associated with
vesicoureteral reflux (VUR) and thought to be congenital. Most female infants do not have demonstrable scarring on initial
imaging, but they subsequently develop it. Delay in treatment of cystitis or pyelonephritis, recurrent UTIs, urinary obstruction,
and VUR increase the risk of scarring.

Acute pyelonephritis (single episode; first UTI ever in one half of cases) in an adult woman leads to renal scarring in 46%, as
demonstrated by scintigraphic scanning 10 years later. Subsequent UTIs do not appear to affect the risk of future scarring.

Renal scarring has been demonstrated to be 4 times more likely after pyelonephritis in pregnant women than in nonpregnant
women. In addition, acute pyelonephritis during pregnancy is associated with the following complications:

Acute renal dysfunction (elevated creatinine) in 2% of cases (20-25% in the past)

Acute renal failure in 0.03% of cases

Acute respiratory distress syndrome (bilateral chest radiograph infiltrates and hypoxemia without pulmonary
hypertension) in 1-8% of cases

Low birth weight (< 2500 g) in 7% of cases

Preterm delivery (< 37 wk gestation) in 5% of cases (6-50% in the past)

Recurrence prior to delivery in 18-20% of cases

Sepsis (positive blood cultures) in 17% of cases

Renal transplant pyelonephritis


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Acute renal transplant pyelonephritis occurring in the first 3 months after transplant has a significant association with graft loss
(>40%) by 96 months, as compared with all renal transplant cases with or without the occurrence of pyelonephritis at any time
after the transplant up to 96 months (25-30%).

Patient Education
Patients must take antibiotics as directed and complete the course as prescribed. This minimizes the risk of recurrence and the
development of resistant organisms.

Patients should be advised to drink plenty of fluids, as avoidance of dehydration is important for both patient well-being and
kidney function. When under stress, men typically drink only enough liquid to replace two thirds of the loss. When ill, individuals
drink less and predispose themselves to dehydration. Unavoidable daily water loss is 1.5 L, of which approximately 500 mL is
replaced by the oxidation of carbohydrates. Because patients cannot measure urine specific gravity at home, they should drink
enough water or other liquid to produce light-colored urine, almost like water.

For patient education information, see the Kidneys and Urinary System Center, as well as Urinary Tract Infections and Blood in
the Urine.

Presentation

History
The classic presentation in acute pyelonephritis is the triad of fever, costovertebral angle pain, and nausea and/or vomiting.
These may not all be present, however, or they may not occur together temporally. Symptoms may be minimal to severe and
usually develop over hours or over the course of a day. Infrequently, symptoms develop over several days and may even be
present for a few weeks before the patient seeks medical care. Symptoms of cystitis may or may not be present to varying
degrees. These may include urinary frequency, hesitancy, lower abdominal pain, and urgency.

Gross hematuria (hemorrhagic cystitis) is present in 30-40% of pyelonephritis cases in females, most often young women.
Gross hematuria is unusual in males and should prompt consideration of a more serious cause.

Pain may be mild, moderate, or severe. Flank pain may be unilateral or sometimes bilateral. Discomfort or pain may be present
in the back (lower or middle) and/or the suprapubic area. Patients may describe suprapubic symptoms as discomfort,
heaviness, pain, or pressure. Upper abdominal pain is unusual, and radiation of pain to the groin is suggestive of a ureteral
stone.

Fever is not always present. When present, it is not unusual for the temperature to exceed 103°F (39.4°C). The patient may
demonstrate rigor, and chills may be present in the absence of demonstrated fever. Malaise and weakness may also be present.

Gastrointestinal symptoms vary. Anorexia is common. Nausea and vomiting vary in frequency and intensity from absent to
severe. Diarrhea occurs infrequently.

The classic signs and symptoms observed in adults are often absent in children, particularly neonates and infants. In children 2
years of age and younger, the most common symptoms of urinary tract infection (UTI) are failure to thrive, feeding difficulty,
fever, and vomiting. When fever is present, pyelonephritis should be in the differential diagnosis.

Elderly patients may present with typical manifestations of pyelonephritis, or they may experience fever, mental status change,
decompensation in another organ system, or generalized deterioration.

Complicated pyelonephritis

A history of the following indicates an increased risk of complicated pyelonephritis:

Structural abnormalities of the urinary tract

Functional abnormalities of the urinary tract

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Metabolic abnormalities predisposing to UTIs

Recent antibiotic use

Recent urinary tract instrumentation

The presence of any one of the above complicating factors should raise the clinician’s index of suspicion. In many instances,
more than one complicating factor is involved. In addition, if the patient is male, elderly, or a child or has had symptoms for more
than 7 days, the infection should be considered complicated until proven otherwise.

Physical Examination
The patient may or may not have a fever. If fever is present, the temperature may be greater than 103°F (39.4°C). In contrast,
the temperature may be subnormal in patients with associated sepsis. Tachycardia may or may not be present, depending on
associated fever, dehydration, and sepsis.

Blood pressure is usually within the reference range, unless the patient has underlying hypertension, in which case the pressure
may be elevated above the patient's baseline. A systolic blood pressure below 90 mm Hg suggests shock secondary to sepsis
or perinephric abscess.

The patient's appearance is variable. Most commonly, the patient is uncomfortable or appears ill. Patients usually do not have a
toxic appearance, unless there is an underlying problem, such as sepsis, perinephric abscess, or significant dehydration.

On abdominal examination, suprapubic tenderness usually ranges from mild to moderate without rebound. Abdominal
tenderness other than in the suprapubic area suggests another diagnosis. Patients usually do not have rigidity or guarding, and
bowel sounds are often normally active.

Flank or costovertebral angle (CVA) tenderness is most commonly unilateral over the involved kidney, although bilateral
discomfort may be present. Discomfort varies from absent to severe. This finding is usually not subtle and may be elicited with
mild or moderately firm palpation.

In women, a pelvic examination should be performed. Tenderness of the cervix, uterus, and adnexa should be absent. Any
positive finding suggests an additional or alternative diagnosis. If any doubt remains as to the diagnosis, if any signs or
symptoms of urethritis or vaginitis are present, or if a history of dyspareunia is present, a gynecologic cause of the symptoms
should be pursued.

Complications
Complications occur more often in patients with diabetes mellitus, chronic kidney disease, sickle cell disease, renal transplant
(particularly during the first 3 months), AIDS, and other immunocompromised states. It can sometimes be difficult to determine
whether the entities listed below are occurring as a complication of pyelonephritis or are occurring in the absence of
pyelonephritis but with signs and symptoms suggestive of pyelonephritis. The important point is to have a high index of
suspicion for these complications.

Complications may involve any of the following:

Acute kidney injury


Chronic renal damage leading to hypertension and renal failure
Sepsis syndromes
Renal papillary necrosis
Xanthogranulomatous pyelonephritis

Abscesses

Abscesses may include renal cortical abscess, renal corticomedullary abscess, or perinephric abscess. Older adults have a
higher incidence of renal corticomedullary abscesses, which affect men and women equally.

Corticomedullary abscess
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Patients with renal corticomedullary abscesses often present with chills, fever, and flank or abdominal pain, and patients may
have dysuria and/or nausea and vomiting. Leukocytosis may be present. Bacteriuria, pyuria, hematuria, or proteinuria may be
present, as the intrarenal abscesses drain in the collecting system, but the urinalysis results may be normal in as many as 30%
of patients. Bacteremia may be observed in acute focal or multifocal bacterial nephritis.

Corticomedullary abscess is usually associated with a urinary tract abnormality, such as vesicoureteral reflux or obstruction. It is
commonly caused by Enterobacteriaceae.

The pathology represents a spectrum of disease, as follows:

Acute focal bacterial nephritis (eg, acute lobar nephroma, focal pyelonephritis) that affects a single renal lobe, with
interstitial inflammation represented by marked polymorphonuclear leukocytes

Acute multifocal bacterial nephritis, with a similar process throughout the kidney that produces liquefaction and abscess
formation

Xanthogranulomatous pyelonephritis, with chronic parenchymal infection, granulomatous tissue, and perirenal fibrosis

Emphysematous pyelonephritis, with severe, necrotizing infection

Perinephric abscess

The suppurative material of the abscess is located between the renal capsule and the surrounding renal fascia. The material is
secondary to chronic or recurrent pyelonephritis; rupture or extension of a suppurative process from within the kidney; or
dissemination (blood, lymph) or direct extension from other sites of infection. Although it is usually confined to the perinephric
space, it may extend to the colon, flank, groin, lung (empyema, nephrobronchial fistula), paracervical area, peritoneal cavity,
psoas muscle, skin surface, or subphrenic space.

Development is insidious. Presentation may include the following:

Fever
Chills
Unilateral flank pain (70%)
Dysuria (40%)
Nausea
Vomiting
Weight loss (25%)
Flank tenderness
Costovertebral angle tenderness
Abdominal tenderness (60%)
Referred pain (ie, hip, thigh, or knee)
Flank or abdominal mass (< 50%)
Pyuria (70%)
Sterile urine (40%)
Bacteremia (40%)
Curvature of the spine away from the involved kidney

One third of patients are diagnosed upon admission; another third are diagnosed at autopsy. Perinephric abscess is not usually
readily apparent; a high index of clinical awareness is necessary.

Renal cortical abscess

Renal cortical abscess (renal carbuncle) is an uncommon condition that is usually caused by the hematogenous spread of S
aureus. It occurs 3 times more commonly in men than in women. Microabscesses develop in the cortex and coalesce to form a
circumscribed abscess that may or may not communicate with the collecting system. This process takes days to months.

Patients with renal cortical abscess may present with chills, fever, and flank or abdominal pain. A flank mass or a bulge in the
lumbar region may be evident. Some patients have abnormal results on lung examination of the affected side (dullness to
percussion, rales). Blood and urine culture results usually are negative, but the white blood cell (WBC) count is often elevated.

Emphysematous pyelonephritis, pyelitis, and cystitis

Emphysematous pyelonephritis, which most commonly occurs in patients with diabetes, is a severe, necrotizing form of acute
multifocal bacterial nephritis with extension of the infection through the renal capsule. This leads to the presence of gas within
the kidney substance and in the perinephric space. Persons with diabetes (with or without obstruction) account for 85-100% of
cases, although some cases have occurred in patients without diabetes who had obstruction. Females outnumber males (2-
6:1).
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Emphysematous pyelonephritis occurs in the left kidney in approximately two thirds of cases. The etiology is usually
Enterobacteriaceae (E coli, 60%), with some reported cases of Streptococcus species and Candida species. A triad of diabetes,
obstruction, and remote or recent pyelonephritis should raise clinical suspicion. Patient presentation includes fever, chills,
abdominal pain, nausea, vomiting, flank pain, flank mass (50%), crepitation (over thigh or flank), urinary symptoms, and pyuria.

Emphysematous pyelitis (pneumopyonephrosis) involves gas that is localized to the collecting system. Diabetes mellitus is
present in 85-100% of patients. The left kidney is more frequently affected than the right. Presentation is similar to that of
pyelonephritis. On plain radiographs, the gas pattern is noted in the renal pelvis and may be seen in the ureter. The patient
should be admitted and treated with intravenous antibiotics. The mortality rate is 20%.

Emphysematous cystitis (cystitis emphysematosa) involves gas that is localized to the bladder secondary to a bladder infection.
Gas in the bladder is more frequently related to a fistula between the bladder and the colon or vagina than to a gas-producing
infection. As many as 80% of patients are diabetic.

Patient presentation is similar to that for pyelonephritis. Plain radiographs may demonstrate gas in the bladder wall or lumen, an
air-fluid level in the bladder, or a cobblestone appearance to the bladder wall. CT scan is the study of choice to help localize the
gas to the proper organ. Treatment involves intravenous antibiotics and relief of any outlet obstruction. This condition is not as
serious as the other two previously described emphysematous conditions.

Xanthogranulomatous pyelonephritis

Xanthogranulomatous pyelonephritis is a rare form of pyelonephritis that is almost always associated with chronic obstruction
(eg, from staghorn calculus [75% of cases], other calculus, stricture, or tumor). In adults, the female-to-male ratio is 3:1; in
children, it is 1.1:1. It is a chronic infection that finally manifests acutely with fever and flank pain or tenderness, and it may be
complicated by a flank mass, cutaneous fistula, septic arthritis, or hematochezia if extension has occurred beyond the renal
capsule. Kidney function is absent (71%) or poor (25%) in almost all cases. Diagnosis is difficult preoperatively.

Tuberculosis

Tuberculosis (TB) of the kidney results from hematogenous spread but is relatively rare in developing countries. Unlike most
other extrapulmonary manifestations of the disease, TB of the kidney does not become manifest until 5-15 years after the
primary infection. Constitutional symptoms are uncommon, and most patients present with symptoms of bladder irritation.

Initially, pyuria is observed, and with progression of the disease, proteinuria and blood may be observed as well. Repeated urine
samples should be sent for mycobacterial culture. A loss of calyceal architecture and ureteric obstruction may be observed on
imaging studies.

Concurrent pulmonary disease is present in 5% of patients, and the tuberculin test rarely is helpful. Antituberculous medicines
should be administered for 6 months. If the ureter is obstructed, corticosteroids have been advocated; if obstruction persists,
surgical intervention is necessary.

DDx

Differential Diagnoses
Acute Abdomen and Pregnancy

Acute Bacterial Prostatitis

Appendicitis

Cervicitis

Chronic Bacterial Prostatitis

Chronic Pyelonephritis

Urinary Tract Infection (UTI) and Cystitis (Bladder Infection) in Females

Endometritis

Pelvic Inflammatory Disease

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Urethritis

Workup

Workup

Approach Considerations
In the outpatient setting, pyelonephritis is usually suggested by the history and physical examination and supported by urinalysis
results, which should include microscopic analysis. Other laboratory studies are used to identify complicating conditions and to
assist in determining whether the patient should be admitted.

Easily diagnosed cases typically occur in women, both pregnant and nonpregnant.[9] Insidious onset may occur in the following:

Men
Patients at the extremes of age
Patients harboring subclinical pyelonephritis
Hospitalized patients

Imaging studies may be required to make the diagnosis in infants and children in whom pyelonephritis presents insidiously.
Imaging studies are rarely indicated for the diagnosis of acute pyelonephritis in an adult who presents with typical signs and
symptoms, but they may be warranted if the presentation is atypical or confusing. Imaging is also warranted if the patient
deteriorates or does not respond to therapy, in which case the important considerations are nephrolithiasis, obstructive uropathy,
and perinephric abscess.

Collection of Urine Specimens


Urine specimens obtained for urinalysis and culture should approximate the urine contained in the bladder as closely as
possible. The procedures for collecting such a urine specimen are as follows:

Clean catch
Urethral catheterization
Suprapubic needle aspiration

Clean catch

When properly collected, a clean-catch specimen adequately reflects the microbiology of the urine in the bladder. This technique
can be performed by ambulatory females aged 6 years and older who do not have any limiting physical handicap.

Importantly, female patients should wash only the area where urine is passed, wash front to back, hold the cup by the outside,
and keep the labia spread while collecting the urine. This is to ensure that the urine goes into the cup without touching the labia.
The presence of a large number of epithelial cells on microscopic examination suggests that the specimen is not a true clean
catch and is unreliable for culture because of contamination with vaginal contents.

Clean-catch technique can also be performed by ambulatory males aged 6 years and older who do not have any limiting
physical handicap. Specimens are usually reliable. Importantly, the patient should clean the head of the penis, retract the
foreskin (if uncircumcised), maintain a good stream, and hold the cup by the outside. In the presence of epispadias or
hypospadias, care must be taken to maintain a good stream while collecting the specimen.

Urethral catheterization

Catheterization poses a small risk of introducing bacteria into the normally sterile bladder environment. Circumstances that
justify this risk when a urine culture is necessary include the following:

Inability to void, or difficulty voiding urine even with hydration


Marked obesity or redundant labia in females
Ill patients who cannot reliably perform the procedure
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Performance of a urologic procedure during which a specimen can be collected
Children 2-6 years of age (if a clinician-assisted clean-catch specimen cannot be collected)

For details on performing this procedure, see Urethral Catheterization in Women and Urethral Catheterization in Men.

Suprapubic needle aspiration

Suprapubic needle aspiration is rarely necessary. Indications are as follows:

An alternative is lacking
To exclude contamination from other methods of collection
To verify the presence of an infecting organism that is otherwise considered a contaminant
To verify infection in an infant who has a positive culture result from a specimen obtained from a strap-on device

For details on performing this procedure, see Suprapubic Aspiration.

Urinalysis
Pyuria is defined as more than 5-10 white blood cells (WBCs) per high-power field (hpf) on a specimen spun at 2000 rpm for 5
minutes. Almost all patients with pyelonephritis have significant pyuria (>20 WBCs/hpf), although the numbers may be smaller,
particularly in those with subacute pyelonephritis.

The dipstick leukocyte esterase test (LET) helps screen for pyuria. LET results have a sensitivity of 75-96% and a specificity of
94-98% for detecting more than 10 WBC/hpf.

The nitrite production test (NPT) for bacteriuria has 92-100% sensitivity and 35-85% specificity. It may be falsely negative in the
presence of diuretic use, low dietary nitrate, or organisms that do not produce nitrate reductase (eg, Enterococcus,
Pseudomonas, Staphylococcus). Combined, the LET-NPT has a sensitivity of 79.2% and a specificity of 81%, which is too low
for it to be used as the only screening study for bacteriuria.

Gross hematuria occurs infrequently with pyelonephritis and is more common with cystitis (hemorrhagic cystitis). When gross
hematuria is present, the differential should include calculi, cancer, glomerulonephritis, tuberculosis, trauma, and vasculitis.

Microscopic hematuria may be present in patients with uncomplicated acute pyelonephritis, but other causes should be
considered, particularly calculi. This is especially true if the patient does not respond to therapy. White cell casts are suggestive
of pyelonephritis; however, centrifuge speeds (>2000 rpm) used for urinalysis sediment preparation often fracture them and lead
to their absence in the sediment.

Proteinuria is expected (up to 2 g/day). When it exceeds 3 g/day, glomerulonephritis should be considered.

The presence of a single bacterium in an unspun urine specimen by oil-immersion microscopic examination is equivalent to at
least 105 colony-forming units (cfu)/mL. Bacteria are identified much more easily on a stained versus an unstained specimen.

Urinary neutrophil gelatinase-associated lipocalin

Urinary neutrophil gelatinase-associated lipocalin (NGAL) is a sensitive biomarker for the diagnosis of acute pyelonephritis in
children. In a case-control study of 134 children with acute pyelonephritis or febrile states of other etiology, NGAL values were
significantly higher in children with acute pyelonephritis. At a cut-off value of 29.4 ng/mL, urinary NGAL had 92.5% sensitivity
and 90.7% specificity for diagnosing acute pyelonephritis. NGAL was also useful for differentiating acute pyelonephritis from
cystitis and differentiating cystitis from febrile states with etiology other than UTI.[10]

Urinary concentrations of NGAL may also help identify children with acute pyelonephritis who are at increased risk of developing
renal scarring. In a study of 54 children, urinary NGAL levels were significantly higher in patients with acute pyelonephritis with
scarring than in those without scarring. At a cut-off value of 7.32 ng/ml, the sensitivity and specificity of this marker for
diagnosing scar formation were 81.3% and 66%, respectively.[11]

Urine and Blood Cultures


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Urine culture is indicated in any patient with pyelonephritis, whether treated in an inpatient or an outpatient setting, because of
the possibility of antibiotic resistance. Reliable results require proper specimen collection.

Blood cultures are indicated in any patient who is being admitted or who has already been admitted. Approximately 12-20% of
patients have cultures that are positive for infection. Bacteremia has not been associated with a poor outcome unless sepsis or
another significant comorbidity is present.

Indications for Imaging Studies


Imaging may be required to make the diagnosis in infants and children in whom pyelonephritis presents insidiously. Imaging is
warranted at the time of admission in patients with the following conditions:

AIDS
Poorly controlled diabetes
Organ transplant (particularly renal)
Other immunocompromised state
Sepsis syndrome
Septic shock

Imaging early in the presentation of acute pyelonephritis may be more useful than previously thought. In one study, 16% of
patients admitted for acute pyelonephritis were found to have new and clinically significant abnormalities on renal imaging at the
time of admission. Later in the hospital course, imaging studies are used for the prompt evaluation of a potentially organ- or life-
threatening complication.

Indications for imaging studies are as follows:

Fever or positive blood culture results that persist for longer than 48 hours
Sudden worsening of the patient’s condition
Toxicity persisting for longer than 72 hours
Complicated UTI

After acute pyelonephritis has resolved, imaging studies may be used during a follow-up examination to identify urinary tract
abnormalities that can predispose the patient to infection. In addition, studies may be used in conjunction with urologic
procedures, including cystoscopy.

Computed Tomography
Contrast-enhanced helical/spiral computed tomography (CECT) is the imaging study of choice, both in adults and in children
with acute pyelonephritis. CECT is more sensitive than ultrasonography and intravenous pyelography (which has only 25%
sensitivity), and it can more readily identify alterations in renal parenchymal perfusion, alterations in contrast excretion,
perinephric fluid, and nonrenal disease.

Noncontrast helical/spiral CT findings may be normal in acute pyelonephritis with mild parenchymal involvement, but the
findings are usually positive when the involvement is moderate or severe. It is the standard study for demonstrating gas-forming
infections, hemorrhage, inflammatory masses, and obstruction.

If findings are suggestive of nephrolithiasis complicating the presentation, a noncontrast CT scan of the kidneys, ureters, and
bladder (KUB) or a CT urogram should be obtained to exclude the possibility of obstruction or hydronephrosis.[12] CT has 97%
accuracy in identifying renal stones. (See the images below.)

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Nonobstructing distal left ureteral calculus 2 X 1 X 2 cm.

Bilateral hydronephrosis.

Abscesses should appear on CT scans as low-density masses with contrast enhancement of the wall from inflamed/dilated
blood vessels (see the image below). Acute focal bacterial nephritis has a lobar distribution of inflammation, wedge-shaped
hypodense lesions (postcontrast), and masslike hypodense lesions in severe infections. Xanthogranulomatous pyelonephritis
may have the following CT features:

Large renal calculi


Nonfunctioning kidneys
Contrast enhancement around low-attenuation areas
Thickening of the Gerota fascia
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Spherical areas of low attenuation

Multiple abscesses, upper pole of left kidney.

Magnetic Resonance Imaging


Magnetic resonance imaging (MRI) can detect renal infection or masses and urinary obstruction, and it can evaluate the renal
vasculature. American College of Radiology Appropriateness Criteria list CT, MRI, and ultrasound as the primary imaging
modalities used in patients with acute pyelonephritis.[13]

A study of diffusion-weighted MRI found that MRI had higher sensitivity than CT (with or without contrast) for the diagnosis of
acute pyelonephritis, and could differentiate areas of nephritis and renal abscesses. However, MRI was less useful than CT for
the diagnosis of renal calculi and emphysematous pyelonephritis.[14]

As there is no radiation exposure, MRI can be used in pregnancy.[15] The cost and availability of MRI remain concerns,
however.[15]

Ultrasonography
Ultrasonography (US) can sometimes detect acute pyelonephritis, but a negative study does not exclude the possibility. Power
Doppler US is superior to color Doppler US in the detection of pyelonephritis but remains inferior to contrast-enhanced
helical/spiral computed tomography (CECT).

Renal US is nevertheless a useful imaging modality in patients with complicated UTIs, and it may be performed at the bedside in
a patient who is hemodynamically unstable. It is relatively inexpensive, it does not involve radiation, and iodinated contrast is not
needed. It is an alternative to CT to identify hydronephrosis if there is concern regarding nephrolithiasis.[12] US is useful in
screening for urinary obstruction in children admitted for febrile illnesses.

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In a study of 207 patients with acute pyelonephritis, Enikeev et al reported that the main findings on ultrasonography were the
following[16] :

Decreased mobility of the kidney


Enlargement of the kidney
Thickened parenchyma
Hydrophilic parenchyma
Impairment of corticomedullary differentiation

On ultrasonography, a renal abscess may appear as a fluid-filled mass with a thick wall. Acute focal bacterial nephritis appears
as a poorly defined mass with low-amplitude echoes and disruption of the corticomedullary junction. In xanthogranulomatous
pyelonephritis, imaging reveals stones in approximately 70% of patients.

Ultrasonographic findings may be falsely negative in 36% of cases of perinephric abscesses. A drawback to ultrasonography is
the difficulty in differentiating renal abscess from tumor; it also is difficult to interpret in a patient who is obese. Renal
angiography may help differentiate renal abscess from renal tumor because an abscess often has increased peripheral
vascularization (the remainder of the mass is avascular).

Scintigraphy
Scintigraphy with technetium-99m dimercaptosuccinic acid (99mTc-DMSA) is almost as sensitive clinically as contrast-enhanced
helical/spiral computed tomography (CECT) in detecting focal renal abnormalities during acute pyelonephritis in adults. DMSA is
a radiotracer that localizes to the renal cortex. This modality is not used much in adults, however, because the findings are not
specific; focal abnormalities may indicate abscess, cyst, infarct, pyelonephritis, or tumor. Additionally,99mTc-DMSA scintigraphy
is much less available in the acute setting than CECT.

In children, however,99mTc-DMSA scintigraphy is the preferred study, because it involves less radiation exposure than CT
scans. It is excellent for helping detect inflammation, scarring, and the distribution of renal function between kidneys.

In pediatric studies, diffusion-weighted magnetic resonance imaging (DW-MRI) compares favorably with 99mTc-DMSA
scintigraphy. A study in seven children with acute pyelonephritis diagnosed on scintigraphy within 7 days of fever onset found
that whole-body non-enhanced DW-MRI had 80% sensitivity and 100% specificity for detecting acute pyelonepritis lesions.[17]

Bosakova et al reported that non-contrast DW-MRI has higher sensitivity than 99mTc-DMSA scintigraphy for
detecting acute renal inflammatory lesions and multifocal lesions in pediatric patients with acute pyelonephritis. Their
prospective study included 31 children aged 3-18 years with a first episode of febrile UTI and without a previously detected
congenital urinary tract malformation, who were evaluated within 5 days of diagnosis. DW-MRI confirmed acute inflammatory
changes of the renal parenchyma, mostly unilateral, in all 31 patients, whereas scintigraphy detected inflammatory lesions in 22
(100% versus 71%; P = 0.002). [18]

CT and MR Urography
CT urography and MR urography are evolving modalities that surpass intravenous urography, which was the prior mainstay of
urinary tract imaging.[19] CT urography provides a detailed anatomic depiction of the urinary tract. MR urography has the
advantage of not using ionizing radiation and has the potential to provide more functional information than CT. However, MR
urography is less established than CT urography and is less reliable in providing diagnostic image quality.[19]

CT urography and MR urography are currently used in the evaluation of hematuria and will become more applicable to the study
of other urologic problems.

Diagnosis of Papillary Necrosis

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Histology and/or imaging studies may help make the diagnosis of papillary necrosis. The sloughed papillae may be obtained by
straining the urine and sending for histology. Retrograde pyelography is the radiologic procedure of choice, but ultrasonography
or CT scan also reveals the diagnosis.

Findings of early renal papillary necrosis include a dilated calyceal fornix, retracted or irregular papillary tip, and extension of
contrast into the parenchyma. A club-shaped cavity in the medulla or papilla may be formed in later disease. When a separated
papilla is surrounded by contrast, a ring may be visualized, which is characteristic of papillary necrosis.

For more information on this topic, see the Medscape Reference article Papillary Necrosis.

Histologic Findings
Features of acute pyelonephritis include suppurative necrosis or abscess formation within the renal substance. In contrast,
features of chronic pyelonephritis (chronic interstitial nephritis) include papillary atrophy and blunting, interstitial fibrosis with
inflammatory infiltrate (ie, lymphocytes, plasma cells, neutrophils [occasional]), tubules (ie, dilated with possible colloid casts,
contracted with atrophy of epithelium), and concentric fibrosis around the parietal layer of the Bowman capsule.

Treatment

Approach Considerations
Ambulatory younger women who present with signs and symptoms of uncomplicated acute pyelonephritis may be candidates
for outpatient therapy. They must be otherwise healthy and must not be pregnant. In addition, they must be treated initially in the
emergency department (ED) with vigorous oral or IV fluids, antipyretic pain medication, and a dose of parenteral antibiotics.
Studies have shown that outpatient therapy for selected patients is as safe as inpatient therapy for a comparable group of
patients and is much less expensive.

Use analgesics as needed. Early in the course of the illness, parenteral analgesics are often necessary to reduce morbidity from
symptoms. Nonsteroidal anti-inflammatory drugs and narcotics are complementary; do not assume that one class is better than
the other.

Admission is usually appropriate for patients who are severely ill, pregnant, or elderly or who have comorbid disorders that
increase the complexity of management or the complication rate (eg, diabetes mellitus, chronic lung disease, congenital or
acquired immunodeficiency). Admission may also be advisable for patients whose social situation is unstable, because of the
possibility of poor compliance or poor follow-up.

Emergency surgery may be indicated in a patient with fever or positive blood culture results persisting longer than 48 hours; in a
patient whose condition deteriorates; or in a patient who appears toxic for longer than 72 hours. These patients may have an
abscess, emphysematous pyelonephritis, or an obstructing calculus. The etiology may not be immediately evident, but an
unexpected change in the clinical picture warrants immediate evaluation for potential surgical intervention.

After recovery from the acute infection, patients may be candidates for elective surgery to reverse conditions that predispose the
kidney to recurrent infections and renal damage. These conditions include congenital anomalies, fistulae involving the urogenital
tract, prostatic hypertrophy, renal calculi, and vesicoureteral reflux.

Antibiotic Selection
Antibiotic selection is typically empirical, because the results of blood or urine cultures are rarely available by the time a decision
must be made. Initial selection should be guided by local antibiotic resistance patterns. Culture results from specimens collected
before the initiation of therapy should be checked in 48 hours to determine antibiotic efficacy.

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The pathogen in community-acquired infections is usually E coli or other Enterobacteriaceae. Accepta ble regimens may include
fluoroquinolones, cephalosporins, penicillins, extended-spectrum penicillins, carbapenems, and aminoglycosides.[20, 3] If
enterococci are suggested on the basis of Gram stain results, ampicillin or vancomycin can replace the fluoroquinolone. If any
doubt exists as to the diagnosis, coverage of both Enterobacteriaceae and enterococci is acceptable.

There is a higher incidence of enterococcal infections in hospitalized and other institutionalized patients. Ampicillin or amoxicillin
should be included in the regimen. If the patient is allergic to penicillin, vancomycin should be substituted.

In choosing an empirical antibiotic regimen, consideration should include the local anti-biogram and drug-resistance rates. For
example, in a community with growing fluoroquinolone resistance, agents in that class may not be an ideal first-line choice. In
light of increasing resistance, short courses of treatment are preferred. In one clinical trial, a 7-day course of oral ciprofloxacin
was shown to be a safe and successful treatment for acute pyelonephritis in women, including older women and those with
more severe infection.[21]

Patient characteristics should also be considered. For example, patients who have been frequently exposed to antibiotics (eg,
solid-organ transplant and hematopoietic transplant patients) or are from institutional facilities are at a greater risk for infection
with drug-resistant pathogens, such as extended-spectrum beta-lactamase–producing or carbapenemase-producing organisms.

For more information, see Pyelonephritis Empiric Therapy and Pyelonephritis Organism-Specific Therapy

Oral versus parenteral administration

Growing data suggest that oral antibiotic therapy, parenteral antibiotic therapy, and initial parenteral antibiotic therapy followed
by oral antibiotic therapy are equally effective regimens, although most of the studies have been small.[22, 23] Some clinicians
believe that initiating therapy with an intravenous or intramuscular dose of medication reduces the risk of therapeutic failure;
other clinicians believe that a completely oral course is sufficient. Data exist to support both assertions.

One conventional regimen comprises levofloxacin, 500 mg/day, given intravenously and then orally for 7-14 days. A short-
course regimen of intravenous levofloxacin at 750 mg/day for 5 days proved non-inferior to that conventional regimen in a
prospective, open-label, randomized, controlled clinical trial in 317 Chinese patients with complicated urinary tract infections and
acute pyelonephritis.[24]

To be considered for oral therapy, patients must meet several prerequisites. They must, of course, be able to tolerate oral
medication. In addition, they must have no indication for admission, and close monitoring to ensure good compliance must be
possible.

One prospective study supports using oral therapy alone in patients who can tolerate oral intake, lack signs of sepsis, and do
not show signs of obstruction or renal suppuration on urinary tract ultrasonography. Another study (prospective, randomized,
unblinded) in a controlled hospital setting found no difference in efficacy between oral and intravenous ciprofloxacin for the initial
management of severe pyelonephritis.

The 2010 IDSA guidelines recommend that women with pyelonephritis who require hospitalization be treated initially with an
intravenous antimicrobial regimen. The choice of antimicrobial agents should be based on local resistance data, with the
regimen tailored on the basis of susceptibility results.[3]

Although the guidelines recommend either 14 days of trimethoprim-sulfamethoxazole (TMP-SMX) or 7 days of ciprofloxacin for
the treatment of pyelonephritis, a study in 272 women with susceptible E coli pyelonephritis reported similar clinical outcomes
with 7 days of TMP-SMX therapy compared with 7 days of ciprofloxacin.[25]

Because of the high rate of resistance of E coli, the empirical use of TMP-SMX should be avoided in patients who require
hospitalization. If beta-lactam drugs and fluoroquinolones are contraindicated, administer aztreonam parenterally. As such, the
patient will need to be admitted.

Regimens for complicated cases

With complicated acute pyelonephritis, treat patients parenterally until defervescence and improvement in the clinical condition
warrants changing to oral antibiotics. Complete the course of therapy with an oral agent selected on the basis of culture results.
[23] Acceptable regimens include the following:

Ampicillin and an aminoglycoside


Cefepime
Imipenem
Meropenem
Piperacillin-tazobactam
Ticarcillin-clavulanate
Ceftazidime-avibactam [26, 27]

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Meropenem-vaborbactam

If the patient is allergic to penicillin, vancomycin should be substituted. Vancomycin or linezolid are options if enterococci are a
consideration.

Meropenem-vaborbactam (Vabomere) is a combination of the carbapenem antibiotic meropenem with the beta-lactamase
inhibitor vaborbactam. Specifically, vaborbactam inhibits bacterial production of the Klebsiella pneumoniae carbapenemase
(KPC) enzyme, which confers resistance to carbapenems.

In August 2017, the US Food and Drug Administration (FDA) approved meropenem-vaborbactam for adults aged 18 years and
older with pyelonephritis and other complicated urinary tract infections caused by designated susceptible Enterobacteriaceae:
Escherichia coli, K pneumoniae, and Enterobacter cloacae species complex.[28]

The safety and efficacy of meropenem-vaborbactam were demonstrated in a study of more than 500 adults with complicated
UTI, including pyelonephritis, in which cure or improvement in symptoms and a negative urine culture were seen in about 98%
of patients treated with meropenem-vaborbactam, versus about 94% of patients treated with piperacillin–tazobactam.
Approximately 7 days after completing treatment, about 77% of patients treated with meropenem-vaborbactam demonstrated
resolution of symptoms and a negative urine culture, compared with about 73% of patients treated with piperacillin–tazobactam.
[28]

Outpatient Treatment
Antibiotic therapy
Patients presenting with acute pyelonephritis can be treated with a single dose of a parenteral antibiotic followed by oral therapy,
provided they are monitored within the first 48 hours. In a study of febrile, nonpregnant women presenting with symptoms of
acute pyelonephritis, 25% were hospitalized; of nonhospitalized patients, 80% were treated with a single parenteral dose of
ceftriaxone or gentamicin, followed by oral therapy (usually trimethoprim-sulfamethoxazole [TMP-SMZ]). Twelve percent
returned with persistent symptoms, most in the first day; most of these were admitted.[5]

Acute pyelonephritis has customarily been treated with 14 days of antibiotics, and 2010 IDSA guidelines maintain this
recommendation for TMP-SMZ and beta-lactam agents. However, evidence suggests that in young, healthy women who are
receiving a fluoroquinolone, including ciprofloxacin, the course of treatment can be shortened to 7 days. Levofloxacin, 750
mg/day, can be given for 5 days.[29, 30] Young, healthy males should complete a 14-day course.[3]

Outpatient treatment is appropriate for patients who have an uncomplicated infection that does not warrant hospitalization. Oral
antibiotics are used to treat patients with mild to moderate illness. (See Table 2, below, for a description of outpatient treatments
for pyelonephritis.)

Table 2. Outpatient Treatment for Pyelonephritis (Open Table in a new window)

First-line therapy

Ciprofloxacin (Cipro) 500 mg PO BID for 7d or

Ciprofloxacin extended-release (Cipro XR) 1000 mg PO daily for 7d or

Levofloxacin (Levaquin) 750 mg PO daily for 5d

If fluoroquinolone resistance is thought to be >10%, administer a single dose of ceftriaxone (Rocephin) 1g IV or a


consolidated 24-hour dose of an aminoglycoside (gentamicin 7 mg/kg IV or tobramycin 7 mg/kg IV or amikacin 20
mg/kg IV)

Second-line therapy
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Trimethoprim/sulfamethoxazole* 160 mg/800 mg (Bactrim DS, Septra DS) 1 tablet PO BID for 14d

If trimethoprim/sulfamethoxazole is used when the susceptibility is not known, an initial single IV dose of the
following may also be given: ceftriaxone (Rocephin) 1 g IV or a consolidated 24-h dose of an aminoglycoside
(gentamicin 7 mg/kg IV or tobramycin 7 mg/kg IV or amikacin 20 mg/kg IV)

Alternative therapy

Oral beta-lactams are not as effective for treating pyelonephritis; however, if they are used, administer with a single
dose of ceftriaxone (Rocephin) 1 g IV or a consolidated 24-h dose of an aminoglycoside (gentamicin 7 mg/kg IV or
tobramycin 7 mg/kg IV or amikacin 20 mg/kg IV)

Amoxicillin-clavulanate (Augmentin) 500 mg/125 mg PO BID for 14d or

Amoxicillin-clavulanate (Augmentin) 250 mg/125 mg PO TID for 3-7d or

Cefaclor 500 mg PO TID for 7d

*Should generally be avoided in elderly patients because of the risk of affecting renal function.

For female patients suspected of having acute pyelonephritis, 2010 guidelines from the Infectious Disease Society of America
(IDSA) recommend sending urine for culture and susceptibility testing and then starting empirical antibiotic therapy.[3]

The fluoroquinolones are well tolerated and quite effective. They are probably the outpatient antibiotic treatment of choice for
pyelonephritis. They (along with TMP-SMZ) do not eradicate the protective lactobacilli from the vagina. An important caveat for
the use of fluoroquinolones in the elderly is their potential to cause a variety of neuropsychiatric symptoms, ranging from
seizures to worsening of dementia.

In communities where the prevalence of resistance in uropathogens to fluoroquinolones is not known to be greater than 10%,
the IDSA guidelines advise that patients who do not require hospitalization be treated with oral ciprofloxacin, 500 mg twice daily
for 7 days, with or without an initial 400-mg dose of intravenous ciprofloxacin. If the uropathogen’s fluoroquinolone resistance is
greater than 10%, an initial intravenous dose of a long-acting parenteral antimicrobial (eg, ceftriaxone, 1 g) is recommended.[3]

On an individual basis, for persons with community-onset UTI and fever, a case-control study found that the risk of
fluoroquinolone-resistant E coli infection increased if the patient had undergone recent hospitalization or urinary catheterization
or if the patient had used a fluoroquinolone within the past 6 months.[22]

IV fluids

If oral intake is not tolerated, intravenous hydration is warranted. Intravenous fluids should include 1 L of 5% dextrose in saline
to reverse any existing ketosis, regardless of whether ketones are detected in the urine. Additional intravenous hydration is
accomplished with normal saline. Exercise caution regarding conditions that might be adversely affected by improper amounts
of fluid, saline, or glucose.

Follow-up

If the patient is not admitted at the time of diagnosis, follow-up reevaluation is important in 1-2 days to be sure the patient is
progressing properly. A good rule based on common sense is that if the managing clinician is concerned that the patient may not
respond well to outpatient management but still thinks the patient deserves a trial at home, the initial follow-up visit should take
place in 24 hours. If the clinician thinks that the patient will do quite well with outpatient management, the initial follow-up visit
can take place in 48 hours.

If the patient thinks that he or she is not progressing well or is getting worse, the patient should be evaluated emergently for
consideration for admission and intravenous antibiotics.

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Continue supportive care by prescribing antiemetics, antipyretics, analgesics, and urinary tract analgesics as needed. Have the
patient complete a 14-day course of oral antibiotics. Evidence suggests that when treating a young, healthy female, the course
of treatment can be shortened to 7 days from 14 days, if the antibiotic being used is a fluoroquinolone. Healthy young males
should complete a 14-day course.

Obtain follow-up urine culture results in any patient with a complicated UTI, a complicated course, or increased risk of infection.
Urine cultures are generally not indicated in healthy, nonpregnant women with resolved symptoms.[9] All patients with a
complicated UTI should be considered for outpatient follow-up imaging of the urinary tract to identify abnormalities that
predispose to further infections.

Rest is essential for recovery. Activity should be minimal. The patient should not return to work for 2 weeks, so as to allow time
for the infection to be eliminated and for the patient to recover physical strength. Temper this recommendation depending on the
physical condition of the patient and the presence of comorbid conditions.

Inpatient Treatment
The decision regarding admission of a patient with acute pyelonephritis depends on age; host factors, such as
immunocompromising chemotherapy or chronic diseases, known urinary tract structural abnormalities, renal calculi, recent
hospitalization, or urinary tract instrumentation; and the patient's response to ED therapy.

Admit all patients with complicated UTI. Complicating factors include the following:

Structural abnormalities (eg, calculi, tract anomalies, indwelling catheter, obstruction)


Metabolic disease (eg, diabetes, renal insufficiency)
Impaired host defenses (eg, HIV, current chemotherapy, underlying active cancer)
Pregnancy

Admission is also indicated for patients with apparent clinically uncomplicated pyelonephritis who have any of the following:

Inability to maintain adequate oral hydration


Evidence of vasomotor instability
Unrelenting fever despite antipyretic therapy
Debilitating pain or dehydration that cannot be corrected promptly in the ED
Inadequate home care or resources to fill prescriptions or comply with the medical regimen (eg, homeless patients,
adolescents, elderly patients in an acute illness setting who are at risk for clouded judgment, patients with substance
abuse issues or other issues that will prevent adequate compliance)

Inpatient care includes the following:

Continue supportive care


Monitor urine and blood culture results
Monitor comorbid conditions for deterioration
Maintain hydration status with IV fluids until hydration can be maintained with oral intake
Continue IV antibiotics until defervescence and significant symptomatic improvement occur; convert to an oral regimen
tailored to urine or blood culture results

In patients with acute pyelonephritis who require hospitalization, treatment begins with intravenous (IV) antibiotics. IV therapy
should be given for 24-48 hours or until severe symptoms improve. A systematic review of 8 randomized, controlled trials in
hospitalized patients with acute pyelonephritis found that early switching to oral antibiotic treatment appears to be as effective
and safe as exclusively IV regimens.[31]

Duration of therapy should be at least 10-14 days, inclusive of initial IV therapy. Patient circumstances may warrant more
prolonged therapy.

Selection of a regimen should be based on local resistance data, and the regimen should be tailored on the basis of
susceptibility results. Recommended regimens are listed in Table 3, below. However, a multinational study in 184 patients found
that cefazolin is non-inferior to ceftriaxone for the empirical treatment of acute pyelonephritis in hospitalized patients. At 72
hours, defervescence or normalization of white blood cell count had occurred in 87.0% of the cefazolin group versus 85.9% of
the ceftriaxone group; in addition, no difference was observed between the two groups for length of stay or 30-day readmission
for cystitis or pyelonephritis.[32]

Table 3. Inpatient Treatment for Acute Pyelonephritis (Open Table in a new window)

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First-line therapy

Ciprofloxacin (Cipro) 400 mg IV q12h for 10-14d or

Levofloxacin (Levaquin) 250 mg IV q24h for 10d or

Levofloxacin (Levaquin) 750 mg IV q24h for 5d

Second-line therapy

Extended-spectrum cephalosporins or penicillins:

Ampicillin-sulbactam (Unasyn) 1.5 g IV q6h or

Piperacillin-tazobactam (Zosyn) 3.375 g IV q6h or

Ticarcillin-clavulanate (Timentin) 3.1 g IV 4-6h or

Cefotaxime (Claforan) 1-2 g IV q8h or

Ceftriaxone (Rocephin) 1 g IV q24h or

Ceftazidime (Fortaz, Tazicef) 2 g IV q8h

All of the above can be administered with or without an aminoglycoside (except in pregnant patients); see
Aminoglycosides, below

Carbapenems:

Meropenem (Merrem) 500 mg IV q8h or

Ertapenem (Invanz) 1 g IV q24h or

Doripenem (Doribax) 500 mg IV q8h

Monobactam (for patients with penicillin allergy):

Aztreonam (Azactam) 1 g IV q8-12h

Alternative therapy

Aminoglycosides (because of their potential nephrotoxicity, aminoglycoside antibiotics should be reserved for patients with
serious and potentially life-threatening infections, and their dosage and blood levels should be carefully monitored to
minimize the risk of nephrotoxicity):

Gentamicin 3 mg/kg/day IV/IM in 3 divided doses or 7 mg/kg/day pulsed dosing or

Tobramycin 3 mg/kg/day IV/IM in 3 divided doses or 7 mg/kg/day pulsed dosing or

Amikacin 10 mg/kg/day IV/IM in 3 divided doses or 20 mg/kg/day pulsed dosing

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Abscesses
For renal cortical abscesses (renal carbuncles), surgical drainage was once the only treatment. However, modern antibiotics
alone often are curative. A semisynthetic penicillin, cephalosporin, fluoroquinolone, or vancomycin is recommended. Generally,
parenteral antibiotics should be administered for 10-14 days, followed by oral therapy for 2-4 weeks. Fever should resolve within
5-6 days, and pain should resolve within 24 hours. If parenteral antibiotic therapy is successful, oral therapy is instituted for an
additional 2-4 weeks.

If patients do not respond within 48 hours, percutaneous (or open) drainage should be performed. Other surgical options are
enucleation of the carbuncle or nephrectomy.

Treatment of renal corticomedullary abscess includes parenteral antibiotics for 48 hours (usually successful), incision and
drainage, and nephrectomy. If antibiotic therapy is successful, oral therapy is instituted for an additional 2 weeks.

Mortality associated with perinephric abscesses is 20-50%, but this rate can be decreased with early recognition, surgical
drainage, and antimicrobial therapy (not adequate alone). Antibiotics should include an aminoglycoside and an
antistaphylococcal agent. If Pseudomonas species are considered or demonstrated, an antipseudomonal beta-lactam antibiotic
should be added. For enterococci, an aminoglycoside and ampicillin are recommended. Other organisms that have been
reported include tuberculosis and fungi. Nephrectomy may be necessary.

Calculi-Related Infections
A major challenge with calculi-related UTI is that the organisms can survive within the calculus. In the presence of acute
infection, calculi must be removed immediately using cystoscopy or open surgical procedure.

The preferred method of treatment is surgical. Options include extracorporeal shockwave lithotripsy (ESWL), endoscopic
methods, percutaneous methods, and open surgery. Mere observation is not recommended, as mortality is 28% with
observation versus 7.2% in the surgically treated group. For staghorn calculus, the treatment of choice is to remove the whole
stone. Fragments left behind remain infected and will grow again. Antibiotic therapy should be used in conjunction.

Although food and vitamin supplements that are rich in phosphorus and magnesium are advisable, remember that magnesium
(and other divalent cations) can chelate fluoroquinolones, preventing their absorption from the gut.

Acidifying agents have been used. Ascorbic acid does not significantly decrease urinary pH, and ammonium chloride provides
only temporary acidification. This approach is of little clinical usefulness. Urease inhibitors are effective in reducing stone
formation, but long-term use is fraught with neurosensory, hematologic, and dermatologic adverse effects.

Other Complicated Infections


Treatment for renal papillary necrosis is admission for intravenous antibiotics. The agents chosen should cover E coli and
Enterobacter, Proteus, and Klebsiella species. Treatment for more serious infections also should cover Pseudomonas and
Enterococcus species.

Parenteral agents that may be used empirically pending the result of a urine culture include the following:

Gentamicin
Cefotaxime
Ceftriaxone
Ceftazidime
Cefepime
Piperacillin-tazobactam
Imipenem-cilastatin
Meropenem
Ciprofloxacin

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Parenteral therapy should be continued until the fever and other symptoms resolve. Duration of therapy generally is 14 days. If
the response is not good, CT-guided drainage or surgical drainage with debridement is indicated.

The treatment of choice for xanthogranulomatous pyelonephritis is nephrectomy after the patient is stabilized. See the
Medscape Reference article Xanthogranulomatous Pyelonephritis for more information.

Pregnant Patients
Physiologic changes in the urinary tract predispose pregnant women to an increased risk of cystitis and pyelonephritis, which
may lead to preterm labor and kidney damage. Hydroureter of pregnancy develops around the seventh week and progresses
throughout the remainder of pregnancy; it resolves by 8 weeks post partum. The ureters may dilate sufficiently to contain 200
mL or more of urine. In addition, the kidneys enlarge and bladder capacity may double. The left kidney is more affected than the
right.

The prevalence of bacteriuria in pregnancy is 2-25%, depending on the study criteria. Symptomatic UTI occurs in 1-3% of all
pregnancies and leads to premature labor in 20-50% of cases.

The recommendation is that all pregnant women have a screening urine culture at 16 weeks' gestation. If the results are
negative for a UTI, no additional cultures are indicated. If the patient has a history of recurrent UTIs, further cultures and other
screening techniques (eg, nitrite dipstick or urine Gram stain) may be needed to detect the development of asymptomatic
bacteriuria.

Accepted regimens for treating asymptomatic bacteriuria include amoxicillin (250 mg orally 3 times a day for 3 or 7 days; or 3 g
in a single dose), cephalexin (2 or 3 g in a single dose), and nitrofurantoin (200 mg in a single dose; or 100 mg 4 times a day for
3 or 7 days). Successful treatment of bacteriuria prevents pyelonephritis. Fluoroquinolones and aminoglycosides should be
avoided in pregnancy. (See Table 4, below, for regimens for pyelonephritis in pregnant patients.)

Inpatient admission is warranted for any pregnant patient with pyelonephritis. The treatment of choice during pregnancy includes
the use of beta-lactam antibiotics. Intravenous antibiotics should be administered until the patient is afebrile for 24 hours and
symptomatically improved. Therapy should be given for 24-48 hours or until severe symptoms improve. Once patients are
afebrile for at least 48 hours, they can be switched to oral antibiotics and discharged to complete 10-14 days of treatment. It is
recommended to avoid fluoroquinolones in pregnant patients. Aminoglycosides should also be avoided due to potential risk of
ototoxicity following prolonged fetal exposure.

Presentation of pyelonephritis is similar in pregnant and nonpregnant females. The antibiotic regimen of choice is intravenous
ampicillin and gentamicin. This is followed by an oral regimen to complete a 14-day course guided by results from susceptibility
studies. Obtain an additional urine culture 1-2 weeks after the completion of therapy to verify eradication of the infection, and
obtain monthly urine cultures until delivery to monitor the urine for recurrent infection.

Postcoital therapy with cephalexin or nitrofurantoin is recommended for prophylaxis against recurrent infection. If the initial
infection requires a second agent for clearing the infection or a recurrent infection occurs, suppressive therapy until delivery is
indicated with nitrofurantoin (50 mg or 100 mg at bedtime). Recurrent infection or persistent bacteriuria is an indication for
urological evaluation 3-6 months after delivery.

Table 4. Treatment of Pyelonephritis During Pregnancy (Open Table in a new window)

Mild to moderate pyelonephritis

Ceftriaxone (Rocephin) 1 g IV q24h or

Cefepime (Maxipime) 1 g IV q12h or

Cefotaxime (Claforan) 1-2 g IV q8h or

Ceftazidime (Fortaz, Tazicef) 2 g IV q8h or

Ampicillin 1-2 g IV q6h plusgentamicin IV 1.5 mg/kg q8h

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Severe pyelonephritis

If patient is immunocompromised and/or has incomplete urinary drainage:

Ticarcillin-clavulanate (Timentin) 3.1 g IV q6h or

Ampicillin-sulbactam (Unasyn) 1.5 g IV q6h or

Piperacillin-tazobactam (Zosyn) 3.375 g IV q6h

Pediatric Patients
In pediatric patients with acute pyelonephritis, indications for immediate urologic referral include the following:

Abnormal electrolyte values associated with acidosis


Elevated blood urea nitrogen level
Hypertension
A palpable bladder
Voiding difficulty (dribbling, poor stream, straining)

Aside from the effects of acute infection, the overriding concern is progressive renal deterioration of an already compromised
kidney (hypoplastic or dysplastic) secondary to scarring from recurrent pyelonephritis with or without associated obstruction. The
groups at greatest risk are infants and preschool-aged children. Initial management varies with patient age and presentation.

Close follow-up examination, regardless of whether the patient is initially admitted, is essential to ensure recovery. Immediate
reevaluation is encouraged for any recurrence of symptoms, because neither treatment of asymptomatic bacteriuria nor long-
term suppressive therapy has been found to be effective.

Urologic evaluation is necessary to establish the presence of any urologic abnormality. The preferred imaging study for the
diagnosis of acute pyelonephritis is technetium-99m dimercaptosuccinic acid (99m Tc-DMSA) scintigraphy. Ultrasonography is
the imaging study of choice for the diagnosis of urinary tract structural abnormalities.

Age-related data adapted from Harwood-Nuss and colleagues and Hansson and colleagues are presented below in Table 5.[33,
34]

Table 5. Pediatric Urinary Tract Infections (Open Table in a new window)

Infants 6 weeks
Neonates to 3 years of Children 3-6 years of age Children 6-11 years of age
age

UTI
frequency 1 1.5-3 1.5-3 1.2
(%)

Female-to-
1:1.5 10:1 10:1 30:1
male ratio

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Route of Blood Ascending Ascending Ascending


infection

Failure to thrive,
Diarrhea, failure Abdominal pain, dysuria,
fever,
to thrive, fever, enuresis, fever, gross
hypothermia, Dysuria, enuresis, fever, flank
Signs and irritability, poor hematuria, meningismus,
irritability, pain or tenderness, urinary
symptoms feeding, strong- strong-smelling urine, urinary
jaundice, poor urgency, urinary frequency
smelling urine, urgency, urinary frequency,
feeding, sepsis,
vomiting vomiting
vomiting

Predominant Klebsiella E coli, Proteus species in


E coli E coli
organism species older boys

Admit for Admit for Follow adult guidelines, but Follow adult guidelines, but
intravenous intravenous avoid fluoroquinolones, which avoid fluoroquinolones, which
ampicillin and ampicillin and are theoretically are theoretically
Management
gentamicin and gentamicin and contraindicated due to contraindicated due to
further further potential effects on the potential effects on the
evaluation evaluation musculoskeletal system musculoskeletal system

Diet and Activity


A regular diet is permitted as tolerated. Special diets, such as those for patients with diabetes mellitus, should be honored.
Maintaining hydration is very important. If admission is not indicated and the patient will be monitored in an outpatient setting,
hydration status should be normalized with intravenous fluids; the physician should not assume that the patient can or will
accomplish this with oral hydration alone.

Rest is essential for recovery. Activity should be minimized. Patients who are treated in an outpatient setting should not return to
work for 2 weeks in order to allow time for the infection to be eliminated. This time also allows the patient to recover physical
strength. This recommendation can be tempered in special circumstances as warranted by the clinician.

Deterrence and Prevention


Prevention of pyelonephritis involves identifying clinical situations that could lead to pyelonephritis and developing a strategy to
decrease that likelihood. These strategies may include a change in contraceptive behavior, administration of prophylactic
antibiotics, or early identification and treatment of cystitis.

If these strategies do not eliminate infection, recurrence of infection, or relapse (reinfection less than 14 days after completing
an appropriate regimen), the patient needs to undergo systematic evaluation for predispositional anatomic, functional, or
structural abnormalities.

For more information, see the Medscape topic Prevention of Urinary Tract Infection (UTI).

Consultations

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Consultation is indicated if the infection is complicated. Most cases of acute pyelonephritis occur in adult women and are readily
managed without consultation. The following are reasons for consulting various subspecialists:

A urologist may be consulted regarding patients with ureteral or urethral obstruction, urinary stones, urogenital
abnormality, or recurrent pyelonephritis, or for the first episode of pyelonephritis in an infant or child

A renal specialist may be consulted regarding patients with acute renal failure or advanced chronic renal failure or for
neonates or infants

An infectious disease specialist may be consulted regarding patients with an unusual or resistant pathogen, those who
are immunocompromised, patients with persisting fever (>48 hours) or toxicity (>72 hours), or patients whose blood
culture results are positive for more than 48 hours

An obstetrician may be consulted for patients who are pregnant

Medication

Medication Summary
Antibiotic therapy is essential in the treatment of acute pyelonephritis and prevents progression of the infection. Urine culture
and sensitivity testing should always be performed, and when results become available, empirical therapy should be tailored to
the infecting uropathogen.[3]

Patients presenting with complicated pyelonephritis should be managed as inpatients and treated empirically with broad-
spectrum parenteral antibiotics. Depending on patient presentation, antibiotic therapy can be completed with oral therapy.
Antibiotics are administered for at least 10-14 days. On the basis of patient presentation, longer duration of therapy may be
needed.

Sulfonamides

Class Summary
Sulfonamides such as trimethoprim-sulfamethoxazole(TMP-SMX) have bacteriocidal activity and are used in the treatment of
pyelonephritis.

Trimethoprim-sulfamethoxazole (Bactrim, Bactrim DS, Septra, Septra DS)


This drug combination is designed to take advantage of the synergy between trimethoprim and sulfonamides. TMP-SMX activity
covers common urinary tract pathogens, both aerobic gram-positive and gram-negative bacteria, except Pseudomonas
aeruginosa.

Oral trimethoprim-sulfamethoxazole (160 mg/800 mg [1 double-strength tablet] twice-daily for 14 days) is an appropriate choice
for therapy if the uropathogen is known to be susceptible. This agent has been given an A-I rating in the 2010 IDSA guidelines
for treating pyelonephritis.

Fluoroquinolones

Class Summary

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Fluoroquinolones are acceptable agents for the treatment of pyelonephritis because they are highly effective against gram-
negative and gram-positive bacteria. A major concern with fluoroquinolones is the development of resistance among
uropathogens and other organisms. Oral fluoroquinolones are a treatment option for patients not requiring hospitalization where
the prevalence of resistance of community uropathogens does not exceed 10%.[3] According to the IDSA 2010 guidelines, if the
prevalence of fluoroquinolone resistance exceeds 10%, an initial 1-time intravenous dose of a long-acting parenteral
antimicrobial or a consolidated 24-hour dose of an aminoglycoside, is recommended.[3] Fluoroquinolones should be avoided
during pregnancy.

Ciprofloxacin (Cipro, Cipro XR)


Oral ciprofloxacin is recommended for patients who do not need hospitalization. Dosing recommendations include 500 mg twice
daily for 7 days, with or without an initial 400-mg dose of intravenous ciprofloxacin. Patients can also be given a once-daily
regimen of ciprofloxacin extended release at a dosage of 1000 mg for 7 days.

Levofloxacin (Levaquin)
Levofloxacin is also recommended as an oral antibiotic for patients with pyelonephritis not requiring hospitalization.
Recommended dose includes the administration of levofloxacin 750 mg for 5 days.

Cephalosporins, Second Generation

Class Summary
Oral beta-lactams are not as effective for treating pyelonephritis. Based on the IDSA 2010 guidelines, however, if they are used,
they should be administered with a single dose of ceftriaxone (Rocephin) 1 g IV ora consolidated 24-hour dose of an
aminoglycoside.[3]

Cefaclor
Cefaclor is indicated for the treatment of pyelonephritis, caused by Escherichia coli, Proteus mirabilis, Klebsiella species, and
coagulase-negative staphylococci. Cefaclor, 500 mg 3 times a day for 7 days, is recommended for outpatient treatment of
pyelonephritis.

Cephalosporins, Third Generation

Class Summary
Third-generation cephalosporins are broad-spectrum and have bactericidal activity. These drugs are the most active against
serious gram-negative pathogens and have some activity against gram-positive pathogens.

Ceftriaxone
Ceftriaxone is a parenteral regimen that can be administered once daily in patients with pyelonephritis requiring hospitalization.
For patients with mild to moderate pyelonephritis, a dosage of 1 g every 24 hours is recommended.

Cefotaxime (Claforan)
Cefotaxime has bactericidal activity. It is indicated for the treatment of genitourinary infections caused by Escherichia coli,
Enterococcus species, and Klebsiella species, among others. For moderate to severe infections, the usual dose is 1-2 g IV or IM
every 8 hours.
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Ceftazidime (Fortaz, Tazicef)


Ceftazidime has broad-spectrum activity against gram-negative organisms, including Pseudomonas, and lower efficacy against
gram-positive organisms. It is approved for the treatment of complicated and uncomplicated cystitis caused by Pseudomonas
aeruginosa; Enterobacter species; Proteus species, including Proteus mirabilis and indole-positive Proteus; Klebsiella species;
and E coli.

Cephalosporins, Other

Class Summary
Cefepime is a fourth-generation drug, which possesses the gram-negative activity of the third-generation agents and the gram-
positive activity of the first-generation drugs.

Cefepime (Maxipime)
Cefepime is a fourth-generation cephalosporin. It is indicated for the treatment of uncomplicated and complicated cystitis,
including (1) pyelonephritis caused by E coli or Klebsiella pneumoniae when the infection is severe or (2) pyelonephritis caused
by E coli, Klebsiella pneumoniae, or Proteus mirabilis when the infection is mild to moderate, including cases associated with
concurrent bacteremia with these microorganisms.

Penicillins, Amino

Class Summary
Aminopenicillins have a broad spectrum of are bactericidal activity against gram-positive and gram-negative organisms.

Ampicillin
Penicillins such as ampicillin can be administered in combination with aminoglycosides for patients with pyelonephritis who
require hospitalization. Ampicillin has bactericidal activity against susceptible organisms.

Amoxicillin-clavulanate (Augmentin, Augmentin XR)


Oral beta-lactams are not as effective for treating pyelonephritis. If they are used, they should be administered with a single
dose of ceftriaxone, 1 g IV, or a consolidated 24-hour dose of an aminoglycoside. Amoxicillin-clavulanate possesses the
properties of a broad-spectrum antibiotic and a beta-lactamase inhibitor.

Penicillins, Extended-Spectrum

Class Summary
Extended-spectrum penicillins have a broad spectrum of bactericidal activity. They are used mainly in the treatment of patients
with pyelonephritis requiring hospitalization.[3] The extended-spectrum penicillins are also an option for pregnant patients with
pyelonephritis.

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Piperacillin-tazobactam (Zosyn)
Piperacillin-tazobactam is useful as empirical therapy before the identification of causative organisms, because of its broad
spectrum of bactericidal activity against gram-positive and gram-negative organisms. The dosing recommendation for severe
pyelonephritis is 3.375 g IV every 6 hours.

Ampicillin-sulbactam (Unasyn)
Ampicillin has a broad spectrum of bactericidal activity against many gram-positive and gram-negative aerobic and anaerobic
bacteria. The presence of sulbactam in the ampicillin-sulbactam formulation effectively extends the spectrum of ampicillin to
include many bacteria normally resistant to it and to other beta-lactam antibiotics. Ampicillin-sulbactam, 1.5 g IV every 6 hours,
can be used for the treatment of pyelonephritis.

Carbapenems

Class Summary
Carbapenem antibiotics are broad-spectrum antibiotics that are structurally related to beta-lactam antibiotics. Carbapenems can
be used in the treatment of patients with pyelonephritis requiring hospitalization.[3] The extended-spectrum penicillins are also
an option for pregnant patients with pyelonephritis.

Doripenem (Doribax)
Doripenem is approved for the treatment of complicated cystitis, including pyelonephritis that is caused by E coli, Klebsiella
pneumoniae, Proteus mirabilis, Pseudomonas aeruginosa, and Acinetobacter baumannii. The usual dosage is 500 mg IV every
8 hours. The duration of therapy can range from 10-14 days. Duration includes a possible switch to an appropriate oral therapy
after at least 3 days of parenteral therapy, once clinical improvement has been demonstrated. Duration can be extended up to
14 days in patients with concurrent bacteremia.

Ertapenem (Invanz)
Ertapenem is approved for the treatment of complicated cystitis, including pyelonephritis caused by Escherichia coli including
cases with concurrent bacteremia or Klebsiella pneumoniae. Usual dosage is 1 g IV every 24 hours for 10-14 days. Duration
includes a possible switch to an appropriate oral therapy after at least 3 days of parenteral therapy, once clinical improvement
has been demonstrated.

Meropenem (Merrem)
Meropenem is a bactericidal broad-spectrum carbapenem antibiotic that is effective against most gram-positive and gram-
negative bacteria. It can be administered at a dose of 500 mg IV every 8 hours.

Imipenem-cilastatin (Primaxin)
Imipenem/cilastatin has bactericidal activity against a wide range of gram-negative and gram-positive organisms. It is an
alternative treatment for pyelonephritis because infections resistant to other antibiotics (eg, cephalosporins, penicillin,
aminoglycosides) have been shown to respond to treatment with imipenem-cilastatin. The general dosing recommendation is
500 mg IV every 6 hours.

Meropenem/vaborbactam (Vabomere)
Indicated for complicated urinary tract infections (cUTI) caused by carbapenem-resistant Enterobacteriaceae (CRE).
Vaborbactam is a non-suicidal beta-lactamase inhibitor that protects meropenem from degradation by certain serine beta-
lactamases such as Klebsiella pneumoniae carbapenemase (KPC). Vaborbactam does not have any antibacterial activity and
does not decrease the activity of meropenem against meropenem-susceptible organisms.
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Aminoglycosides

Class Summary
Aminoglycosides are bactericidal antibiotics used primarily in the treatment of gram-negative infections. They are commonly
used in combination with drugs such as ampicillin. For example, gentamicin, an aminoglycoside antibiotic that has gram-
negative coverage, is used in combination with both an agent against gram-positive organisms and one that covers anaerobes.
Because of their potential nephrotoxicity, aminoglycosides should be reserved as a last resort, for use in resistant or life-
threatening infections. In addition, aminoglycosides should be avoided during pregnancy.

Gentamicin
Gentamicin is not the drug of choice for acute pyelonephritis. Consider using it when penicillins or other less toxic drugs are
contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative
organisms. Dosing regimens are numerous; adjust the dose based on the creatinine clearance and changes in volume of
distribution. Gentamicin may be given intravenously or intramuscularly.

Tobramycin
Tobramycin has bactericidal activity against, and is used to treat infections caused by, E coli, Proteus species, Klebsiella
species, Serratia species, Enterobacter species, and Citrobacter species. Tobramycin can be administered intravenously or
intramuscularly. Dosage is based on weight and renal function.

Amikacin
Amikacin has bactericidal activity against gram-negative organisms. Clinical studies have shown that amikacin is clinically
effective for serious complicated and recurrent cystitis. Amikacin can be administered intravenously or intramuscularly. Dosage
is based on weight and renal function.

Glycopeptides

Class Summary
Glycopeptide antibiotics such as vancomycin have bactericidal activity and can be used as alternative therapy for patients with
pyelonephritis.

Vancomycin (Vancocin)
Vancomycin is a potent antibiotic directed against gram-positive organisms and is active against Enterococcus species.
Vancomycin is indicated for patients who cannot receive or did not respond to penicillins and cephalosporins or patients who
have infections with resistant staphylococci.

Monobactams

Class Summary
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Unlike the penicillins and cephalosporins, aztreonam is a monobactam. Monobactams such as aztreonam are bactericidal;
however, they lack activity against gram-positive activity.

Aztreonam (Azactam)
Aztreonam is approved for the treatment of complicated and uncomplicated cystitis. It is approved for the treatment of
pyelonephritis caused by Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Pseudomonas aeruginosa, Enterobacter
cloacae, Klebsiella oxytoca, Citrobacter species, and Serratia marcescens. Aztreonam lacks cross-sensitivity with beta-lactam
antibiotics and may be used in patients allergic to penicillins or cephalosporins. General dosing recommendations include
administering 1 g IV every 8-12 hours.

Urinary Analgesics

Class Summary
Use of a urinary analgesic is indicated when a patient has dysuria to such an extent that it disrupts activities of daily living.
These agents relieve pain, discomfort, and spasms of the bladder.

Phenazopyridine (Baridium, Pyridium, UTI Relief)


Phenazopyridine is an azo dye excreted in urine, where it exerts a topical analgesic effect on urinary tract mucosa. Its use is
compatible with antibacterial therapy and can help relieve pain and discomfort before antibacterial therapy controls infection.

It is used for symptomatic relief of pain, burning, urgency, frequency, and other discomfort arising from irritation of lower urinary
tract mucosa caused by infection, trauma, surgery, endoscopic procedures, or passage of sounds or catheters. Its analgesic
action may reduce or eliminate the need for systemic analgesics or narcotics.

Questions & Answers


Overview

What is acute pyelonephritis (kidney infection)?

What are the signs and symptoms of acute pyelonephritis (kidney infection)?

What is the occurrence of gross hematuria (hemorrhagic cystitis) in acute pyelonephritis (kidney infection)?

What is the initial course of symptoms of acute pyelonephritis (kidney infection)?

What are the signs and symptoms of acute pyelonephritis (kidney infection) in children?

What are the signs and symptoms of acute pyelonephritis (kidney infection) in elderly patients?

How is acute pyelonephritis (kidney infection) diagnosed?

What is the role of urinalysis in the diagnosis of acute pyelonephritis (kidney infection)?

When is urine culture indicated in patients with acute pyelonephritis (kidney infection)?

What is the role of imaging studies in the assessment of acute pyelonephritis (kidney infection)?

How is acute pyelonephritis (kidney infection) managed?

How is complicated pyelonephritis (kidney infection) managed?

When is outpatient care indicated for the treatment of acute pyelonephritis (kidney infection)?

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What is included in the inpatient care for acute pyelonephritis (kidney infection)?

When is surgery indicated in the management of pyelonephritis (kidney infection)?

What is acute pyelonephritis (kidney infection)?

What is the incidence of acute pyelonephritis (kidney infection)?

Which factors make diagnosis and management of acute pyelonephritis (kidney infection) challenging?

What are the signs and symptoms of acute pyelonephritis (kidney infection)?

How is pyelonephritis identified in women?

What is the presentation of acute pyelonephritis (kidney infection) in elderly patients and infants?

Which signs and symptoms are both sensitive and specific for the diagnosis of acute pyelonephritis (kidney infection)?

What are the effective antibiotic options and therapy duration for acute pyelonephritis (kidney infection)?

Can acute pyelonephritis (kidney infection) be managed successfully on an outpatient basis?

What is complicated pyelonephritis (kidney infection) and how should it be managed?

What is the pathophysiology of acute pyelonephritis (kidney infection)?

What is the role of uropathogenic E coli (UPEC) in the pathogenesis of acute pyelonephritis (kidney infection)?

What is the role of mannose-resistant adhesins in the pathogenesis of acute pyelonephritis (kidney infection)?

What is the role of P fimbriae adhesins in the pathogenesis of acute pyelonephritis (kidney infection)?

What is the role of siderophores and protectins in the pathogenesis of acute pyelonephritis (kidney infection)?

Which toxins have a role in the pathogenesis of acute pyelonephritis (kidney infection)?

Which virulence factors promote the pathogenesis of acute pyelonephritis (kidney infection)?

What is the role of asymptomatic bacteriuria (ABU) strains in acute pyelonephritis (kidney infection)?

Which microorganisms are commonly isolated in acute pyelonephritis (kidney infection)?

What is the 2-step path in the pathogenesis of acute pyelonephritis (kidney infection)?

Which factors reduce the efficacy of antibiotics for complicated urinary tract infection (UTI)?

What is the role of obstruction in the pathogenesis of acute pyelonephritis (kidney infection)?

What is the role of staghorn calculi in acute pyelonephritis (kidney infection)?

What are the adverse effects of untreated staghorn calculi?

Which agent inhibits the growth of lactobacilli?

What predisposes the colonization of urinary tract pathogens in postmenopausal women?

What are the less common organisms in complicated urinary tract infection (UTI)?

What is the role of urea-splitting organisms in complicated urinary tract infection (UTI)?

What are possible complications of obstruction in urinary tract infection (UTI)?

How does pregnancy affect the pathophysiology of acute pyelonephritis (kidney infection)?

How does diabetes mellitus affect the pathophysiology of acute pyelonephritis (kidney infection)?

What is the etiology of acute pyelonephritis (kidney infection)?

What is the incidence of pyelonephritis (kidney infection) in the US?

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What is the prevalence of acute pyelonephritis in pregnant women and infants and children?

What are the race-, sex-, and age-related predilections of acute pyelonephritis (kidney infection)?

Is there seasonal variation in the incidence of acute pyelonephritis (kidney infection)?

What is the prognosis of acute pyelonephritis (kidney infection)?

Does acute pyelonephritis (kidney infection) increase the risk of premature labor?

What are the possible morbidities of acute pyelonephritis (kidney infection)?

What are the mortality and morbidity rates in patients with acute pyelonephritis (kidney infection)?

What is the prognosis of uncomplicated pyelonephritis (kidney infection)?

When does pyelonephritis become a potentially fatal disease?

What are the mortality rates in emphysematous pyelonephritis and emphysematous pyelitis?

What is the mortality rate for patients with sepsis and acute pyelonephritis (kidney infection)?

Can acute pyelonephritis (kidney infection) cause acute renal failure (ARF)?

What is the prevalence of renal scarring in children with acute pyelonephritis (kidney infection)?

What is the prevalence of renal scarring in women with acute pyelonephritis (kidney infection)?

What are the possible complications of acute pyelonephritis (kidney infection) during pregnancy?

Does acute pyelonephritis (kidney infection) after renal transplantation increase the risk of graft failure?

How are antibiotics administered in patients with acute pyelonephritis (kidney infection)?

How does dehydration occur in patients with acute pyelonephritis?

Presentation

What is the typical presentation of acute pyelonephritis (kidney infection)?

What is the prevalence of gross hematuria (hemorrhagic cystitis) in patients with acute pyelonephritis (kidney infection)?

What is the presentation of pain in patients with acute pyelonephritis (kidney infection)?

How is fever characterized in patients with acute pyelonephritis (kidney infection)?

What is the presentation of GI symptoms in patients with acute pyelonephritis (kidney infection)?

What are the signs and symptoms of acute pyelonephritis (kidney infection) in children?

What is the presentation of acute pyelonephritis (kidney infection) in elderly patients?

Which history increases the risk of complicated pyelonephritis (kidney infection)?

What are the physical findings in patients with acute pyelonephritis (kidney infection)?

What are the physical findings of fever in patients with acute pyelonephritis (kidney infection)?

What are blood pressure findings in patients with acute pyelonephritis (kidney infection)?

Which abdominal exam findings indicate acute pyelonephritis (kidney infection)?

How is flank or costovertebral angle (CVA) tenderness characterized in patients with acute pyelonephritis (kidney infection)?

Which pelvic exam findings indicate acute pyelonephritis (kidney infection)?

In which patient groups is the risk for complication increased from acute pyelonephritis (kidney infection)?

What are the possible complications of acute pyelonephritis (kidney infection)?

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Which abscesses may be present in patients with acute pyelonephritis (kidney infection)?

What is the presentation of corticomedullary abscess in acute pyelonephritis (kidney infection)?

What is the pathogenesis of corticomedullary abscess in patients with acute pyelonephritis represent?

What is the presentation of perinephric abscess in acute pyelonephritis (kidney infection)?

What is the prevalence of perinephric abscess in acute pyelonephritis (kidney infection)?

What is the pathogenesis of renal cortical abscess (renal carbuncle) in acute pyelonephritis (kidney infection)?

What is the presentation of renal cortical abscess (renal carbuncle) in acute pyelonephritis (kidney infection)?

What is emphysematous pyelonephritis?

What is emphysematous pyelitis (pneumopyonephrosis)?

What is emphysematous cystitis (cystitis emphysematosa)?

What is xanthogranulomatous pyelonephritis?

What is the presentation of TB in acute pyelonephritis (kidney infection)?

How is TB managed in patients with acute pyelonephritis (kidney infection)?

DDX

What are the differential diagnoses for Acute Pyelonephritis?

Workup

How is acute pyelonephritis (kidney infection) diagnosed?

When is acute pyelonephritis (kidney infection) easily diagnosed and when might it present with an insidious onset?

What is the role of imaging studies in the diagnosis of acute pyelonephritis (kidney infection)?

Which collection methods are used for urine specimens for acute pyelonephritis (kidney infection)?

When is a suprapubic needle aspiration for collecting a urine specimen indicated in the diagnosis of acute pyelonephritis (kidney
infection)?

Who can perform a clean-catch technique for urine sample collection in acute pyelonephritis (kidney infection)?

How is the clean-catch technique for collecting urine specimen performed in female patients with acute pyelonephritis?

How is the clean-catch technique for collecting urine specimen performed in male patients with acute pyelonephritis (kidney
infection)?

When is urethral catheterization for collecting a urine specimen indicated for diagnosis of acute pyelonephritis (kidney
infection)?

How is pyuria defined?

Which tests are used for pyuria screening in the diagnosis of acute pyelonephritis (kidney infection)?

Which disorders should the included in the differential diagnosis acute pyelonephritis when gross hematuria (hemorrhagic
cystitis) is present?

What is the presentation of microscopic hematuria in patients with acute pyelonephritis (kidney infection)?

What is the significance of a proteinuria finding in the urinalysis of patients with acute pyelonephritis (kidney infection)?

What does the presence of a single bacterium in an unspun urine specimen indicate in the evaluation of acute pyelonephritis
(kidney infection)?

What is the role of urinary neutrophil gelatinase-associated lipocalin (NGAL) in the diagnosis of acute pyelonephritis (kidney
infection)?

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When is a urine culture indicated in the evaluation of acute pyelonephritis (kidney infection)?

When is a blood culture indicated in the evaluation of acute pyelonephritis (kidney infection)?

What is the role of imaging studies in the diagnosis of acute pyelonephritis (kidney infection)?

What are the benefits of early imaging in acute pyelonephritis (kidney infection)?

When are imaging studies indicated in the evaluation of acute pyelonephritis (kidney infection)?

How are imaging studies used in the management of acute pyelonephritis (kidney infection)?

What is the imaging study of choice in the evaluation of acute pyelonephritis?

What is the role of noncontrast helical/spiral CT scanning in the evaluation of acute pyelonephritis (kidney infection)?

When is a noncontrast CT scan of the kidneys, ureters, and bladder (KUB) or a CT urogram indicated in the evaluation of acute
pyelonephritis (kidney infection)?

Which CT scan findings indicate complications of acute pyelonephritis?

What is the role of MRI in the evaluation of acute pyelonephritis (kidney infection)?

What is the role of ultrasonography (US) in the evaluation of acute pyelonephritis (kidney infection)?

Which ultrasonography (US) findings indicate complications of acute pyelonephritis?

What are the disadvantages of diagnostic ultrasonography (US) for acute pyelonephritis and when is renal angiography
indicated?

What is the role of scintigraphy in the evaluation of acute pyelonephritis (kidney infection)?

What is the role of CT urography or MR urography in the evaluation of acute pyelonephritis (kidney infection)?

Which studies are helpful in the diagnosis of papillary necrosis in acute pyelonephritis (kidney infection)?

Which findings suggest early renal papillary necrosis in acute pyelonephritis (kidney infection)?

What are the histologic findings of acute pyelonephritis (kidney infection)?

Treatment

When is outpatient therapy indicated for acute pyelonephritis?

What is the role of analgesics in the treatment of acute pyelonephritis (kidney infection)?

When is hospitalization indicated for the treatment of acute pyelonephritis (kidney infection)?

When is emergency surgery indicated for acute pyelonephritis (kidney infection)?

When is elective surgery indicated for acute pyelonephritis (kidney infection)?

How is antibiotic selection guided for acute pyelonephritis (kidney infection)?

Which antibiotics should be used to treat community-acquired acute pyelonephritis (kidney infection)?

Which antibiotics should be used to treat enterococcal infections in hospitalized and other institutionalized patients with acute
pyelonephritis (kidney infection)?

Which factors should be considered when choosing an empirical antibiotic regimen for acute pyelonephritis (kidney infection)?

Is oral administration of antibiotics more effective than other regimens for the treatment of acute pyelonephritis (kidney
infection)?

When is oral therapy indicated for the treatment of acute pyelonephritis (kidney infection)?

What are the IDSA recommendations for inpatient treatment of women with pyelonephritis (kidney infection)?

When should the empirical use of TMP-SMZ be avoided for treatment of acute pyelonephritis (kidney infection)?

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Which antibiotics are used for the treatment of complicated acute pyelonephritis (kidney infection)?

What is the efficacy of antibiotic therapy for acute pyelonephritis treatment?

What is the IDSA recommendation for duration of antibiotic therapy for acute pyelonephritis?

When is outpatient treatment indicated for acute pyelonephritis?

What are the IDSA recommendations for management of a female patient suspected of having acute pyelonephritis (kidney
infection)?

What is the role of fluoroquinolones in the treatment of acute pyelonephritis?

What are the IDSA recommendations for treatment of fluoroquinolone-resistant acute pyelonephritis (kidney infection)?

Which factors increase the risk of fluoroquinolone-resistant E coli infection in patients with acute pyelonephritis (kidney
infection)?

When is IV hydration indicated for the management of acute pyelonephritis?

When is reevaluation of acute pyelonephritis indicated?

What are the supportive care options for acute pyelonephritis (kidney infection)?

When is follow-up testing indicated in the management of acute pyelonephritis?

Should activity be restricted during recovery from acute pyelonephritis (kidney infection)?

Which factors should be considered in the admission decision for patients with acute pyelonephritis (kidney infection)?

Which complicating factors are indications for admission of patients with acute pyelonephritis (kidney infection)?

Which patients with uncomplicated pyelonephritis (kidney infection) should be admitted for inpatient treatment?

What should be included in inpatient treatment of acute pyelonephritis (kidney infection)?

What is the duration of inpatient antibiotic therapy for acute pyelonephritis (kidney infection)?

Which factors should be considered in the selection of an antibiotic regimen for acute pyelonephritis (kidney infection) inpatient
treatment?

What are the treatment options for abscesses in patients with acute pyelonephritis (kidney infection)?

When is surgical treatment of abscesses indicated in patients with acute pyelonephritis (kidney infection)?

What is included in the treatment of renal corticomedullary abscess in patients with acute pyelonephritis (kidney infection)?

What is the mortality rate for perinephric abscesses in patients with acute pyelonephritis (kidney infection)?

What is the treatment for calculi-related infections in patients with acute pyelonephritis (kidney infection)?

What are the advantages and disadvantages of phosphorus and magnesium supplements in the treatment of calculi-related
infections in patients with acute pyelonephritis (kidney infection)?

What are the treatment options for renal papillary necrosis in patients with acute pyelonephritis (kidney infection)?

Which agents are used empirically to treat renal papillary necrosis in patients with acute pyelonephritis?

What is the duration of treatment for renal papillary necrosis in patients with acute pyelonephritis (kidney infection)?

What is the treatment of choice for xanthogranulomatous pyelonephritis?

Which factors increase the risk of pyelonephritis (kidney infection) during pregnancy?

What is the prevalence of bacteriuria and symptomatic urinary tract infection (UTI) during pregnancy?

What is the recommendation for urinary tract infection (UTI) screening in pregnant women?

Which regimens are used for the treatment of asymptomatic bacteriuria during pregnancy?

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What is the treatment for pregnant women with acute pyelonephritis (kidney infection)?

What is the antibiotic regimen of choice for pregnant women with pyelonephritis (kidney infection)?

What therapy is recommended for prophylaxis against recurrent infection in pregnant women with acute pyelonephritis (kidney
infection)?

When is immediate urologic referral indicated for pediatric acute pyelonephritis (kidney infection)?

Which children are at increased risk for complications of acute pyelonephritis (kidney infection)?

Why is follow-up exam essential in pediatric patients with acute pyelonephritis (kidney infection)?

Which imaging studies are preferred for the urologic evaluation of pediatric patients with acute pyelonephritis?

What are age-related data for pediatric patients with acute pyelonephritis (kidney infection)?

Are dietary restrictions needed for pediatric patients with acute pyelonephritis (kidney infection)?

Are activity restrictions needed for pediatric patients with acute pyelonephritis (kidney infection)?

What are the deterrence and prevention strategies for pyelonephritis (kidney infection)?

Which specialist consultations are indicated for acute pyelonephritis (kidney infection)?

Medications

What is the role of urine culture in the treatment of acute pyelonephritis (kidney infection)?

How should patients presenting with complicated pyelonephritis (kidney infection) be managed?

Which medications in the drug class Sulfonamides are used in the treatment of Acute Pyelonephritis?

Which medications in the drug class Fluoroquinolones are used in the treatment of Acute Pyelonephritis?

Which medications in the drug class Cephalosporins, Second Generation are used in the treatment of Acute Pyelonephritis?

Which medications in the drug class Cephalosporins, Third Generation are used in the treatment of Acute Pyelonephritis?

Which medications in the drug class Cephalosporins, Other are used in the treatment of Acute Pyelonephritis?

Which medications in the drug class Penicillins, Amino are used in the treatment of Acute Pyelonephritis?

Which medications in the drug class Penicillins, Extended-Spectrum are used in the treatment of Acute Pyelonephritis?

Which medications in the drug class Carbapenems are used in the treatment of Acute Pyelonephritis?

Which medications in the drug class Aminoglycosides are used in the treatment of Acute Pyelonephritis?

Which medications in the drug class Glycopeptides are used in the treatment of Acute Pyelonephritis?

Which medications in the drug class Monobactams are used in the treatment of Acute Pyelonephritis?

Which medications in the drug class Urinary Analgesics are used in the treatment of Acute Pyelonephritis?

Contributor Information and Disclosures

Author

Tibor Fulop, MD, PhD, FACP, FASN Professor of Medicine, Department of Medicine, Division of Nephrology, Medical University
of South Carolina College of Medicine; Attending Physician; Medical Services, Ralph H Johnson VA Medical Center

Tibor Fulop, MD, PhD, FACP, FASN is a member of the following medical societies: American Academy of Urgent Care
Medicine, American College of Physicians, American Society of Diagnostic and Interventional Nephrology, American Society of
Hypertension, American Society of Nephrology, International Society for Apheresis, International Society for Hemodialysis,
Magyar Orvosi Kamara (Hungarian Chamber of Medicine), Southern Society for Clinical Investigation

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Disclosure: Nothing to disclose.

Specialty Editor Board

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program,
Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff,
Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of
Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American
Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International
Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Society of
Nephrology<br/>Received income in an amount equal to or greater than $250 from: Healthcare Quality Strategies,
Inc<br/>Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of
Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from
University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced
Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for
independent cont.

Chief Editor

Vecihi Batuman, MD, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School
of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians, American Society
of Hypertension, American Society of Nephrology, International Society of Nephrology, Southern Society for Clinical
Investigation

Disclosure: Nothing to disclose.

Acknowledgements

Amy J Behrman, MD Associate Professor, Department of Emergency Medicine, Director, Division of Occupational Medicine,
University of Pennsylvania School of Medicine

Amy J Behrman, MD is a member of the following medical societies: American College of Occupational and Environmental
Medicine

Disclosure: Nothing to disclose.

Christopher Edwards, MD Resident Physician, Department of Emergency Medicine, University of Pennsylvania School of
Medicine

Christopher Edwards, MD is a member of the following medical societies: American College of Emergency Physicians and
Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Judith Green-McKenzie, MD, MPH Associate Professor, Director of Clinical Practice, Occupational Medicine Residency Director,
University of Pennsylvania School of Medicine

Judith Green-McKenzie, MD, MPH is a member of the following medical societies: American College of Occupational and
Environmental Medicine, American College of Physicians, American College of Preventive Medicine, National Medical
Association, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director,
Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville
Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science,
American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for

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Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of
Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Chike Magnus Nzerue, MD Associate Dean for Clinical Affairs, Vice-Chairman of Internal Medicine, Meharry Medical College

Chike Magnus Nzerue, MD is a member of the following medical societies: American Association for the Advancement of
Science, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American
Society of Nephrology, and National Kidney Foundation

Disclosure: Nothing to disclose.

Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM Associate Professor, Education Officer, Department of
Emergency Medicine, Hospital of the University of Pennsylvania; Director of Education and Research, PENN Travel Medicine

Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM is a member of the following medical societies: Alpha Omega
Alpha, American Academy of Emergency Medicine, American Society of Tropical Medicine and Hygiene, International Society of
Travel Medicine, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

William H Shoff, MD, DTM&H Director, PENN Travel Medicine; Associate Professor, Department of Emergency Medicine,
Hospital of the University of Pennsylvania, University of Pennsylvania School of Medicine

William H Shoff, MD, DTM&H is a member of the following medical societies: American College of Physicians, American Society
of Tropical Medicine and Hygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, and
Wilderness Medical Society

Disclosure: Glaxo Smith Kline None None; Glaxo Smith Kline Honoraria Speaking and teaching

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy;
Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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