Jam, Richelle, April, Anne

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IV.1 Nephrology
Dr. Doctor
December 9, 2013
*Normal text = Docs powerpoint
*Italicized text = Notes from lecture
*Text inside dashed boxes = Notes from last years
trans/ Nelson

KIDNEY AND URINARY TRACT
I. KIDNEYS
Nephron
Glomerulus
Tubules - Calyces
Interstitium
Special Cells

II. URETER
III. URINARY BLADDER
Urinary Bladder Junction
Urethral Valve/ Sphincter


Figure 1. Pediatric Urinary Tract
Table 1. Organs of theUrinary Tract and their Functions
PART FUNCTION
Kidneys A pair of organs that filter the
blood of the waste, unused
minerals, and water that make up
urine.
Calyx Small chambers in the kidneys
that drain urine into the renal
pelvis
Renal Pelvis Where urine collects before flowing
down the ureters
Ureters A pair of tubes that carry urine
from the kidneys to the bladder
Bladder An organ that stores urine until
the child is ready to release it.
Ureterovesical
junction
Valve function which is
responsible for protection of the
low pressure upper urinary tract
from the refluxing of urine from
the bladder
Sphincters Ring-shaped bands of muscles.
The urethral sphincters work
together to hold in or release urine
from the bladder. They close and
tighten to hold and open and relax
to release.
Nerves Signal when the bladder is filled
with urine. They also tell the
sphincter and bladder when its
time to empty the bladder.
Urethra Tube that carries urine from the
bladder out of the body

KIDNEYS OF A NEWBORN INFANT
Relatively large and can usually be palpated through
the anterior abdominal wall
Mean combined weight of both kidneys at birth
6 months = 24 g
12 month = 70 g
6 years old = 140 g
Adult weight = 300 g

NEPHRON
Structural and functional unit of the renal parenchyma
At 36th week of gestation, nephrogenesis stops and
each kidney has 850,000 to 1M nephrons
Each nephron consists of glomerulus and its tubules
For urine formation, acid-base balance, secretion of
certain substances
Each glomerulus is made of capillary tufts enclosed
in Bowmans capsule
Capillary tufts consists of loops bound together in a
central area called mesangium
Mesangium is composed of cytoplasmic matrix and
cells (mesangial or capillary); it is usually the first to
react in the event of glomerular insult
3 fixed cells of glomerulus:
Endothelial or intracapillary cell
Mesangial cell
Epithelial or extracapillary cell

3 PRICINCIPLES OF KIDNEY FUNCTION
1. Maintain constancy of internal environment by
adjusting volume, concentration and composition of
body fluids
2. Elimination of metabolic wastes such as urea and
creatinine
3. Elaborate the hormones renin, erythropoietin,
prostaglandin kallikrein-kinin

URINE FORMATION
Initiated by elaboration of a large volume of protein-
free plasma ultrainfiltrate through glomerular filtration
Concentration and alteration of filtrate composition in
the tubules (through tubular reabsorption of essential
substances and elimination of waste products)

PROXIMAL TUBULES
Reabsorbs 80% of filtrate volume and sodium
All the glucose and amino acids (small portion) and
much of the filtered phosphate
Primary active process is Na
+
reabsorption
Followed by passive reabsorption of Cl
-
and H2O by
diffusion
Volume is greatly reduced but Na
+
and Cl
-
not altered

LOOP OF HENLE
Water is reabsorbed in the descending limb
Na
+
is reabsorbed in the ascending limb
Result is an environment in the interstitial tissue of
medulla that is hypertonic to plasma thus urine
concentration takes place in the adjacent collecting
ducts
Fluid at the end of the loop is hypertonic

DISTAL TUBULES
Fluid is initially hypotonic to plasma due to large
amount of Na
+
reabsorbed in the ascending limb
More Na
+
reabsorbed due to aldosterone
K
+
is secreted
Acidification takes place


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COLLECTING DUCT
Final concentration mediated by vasopressin acting on
the lining cells of the duct making them more
permeable to water

Table 2. Glomerulus and Tubules
GLOMERULUS TUBULES
BP, Volume

Concentration

If decreased filtration
decreased blood flow
decreased output
decreased urine volume
Responsible for
increased urine
concentration
Overcrowding/
inflammation
oliguria/anuria
Tubulo-interstitial
nephritis

Additional notes:
Normal Kidney 1M nephrons
Mechanism of Urination:
Gravitational pull of the fluid Detrusor muscle
distention Sphincter opening
Normal GFR
Adult: 100-120 mL/min or approximately 2L
filtration/day
1% goes down as urine (700-1500 mL/day)
Excreted metabolic acids 1 mEq/kg
In children: Ureters are dilated


DIAGNOSTIC MODALITIES
URINALYSIS
Physical
Color
Turbidity
Specific gravity
Acidic/ Basic
Odor
Microscopic
Red Blood Cells (RBC)
White Blood Cells (WBC)
Crystals
Other Cells
Casts
Chemical
Sugar
Protein
Pigments e.g.Bilirubin
Electrolytes Na, K, Cl, Ca, Mg
Ketones appears when you have starvation
Uric acid will predispose to crystal formation
Urea due to high protein intake

ANATOMIC IMAGING
Gross
Ultrasound
o KUB with Prevoid-Postvoid image
X-ray
a. Plain
b.Contrast
o Intravenous Pyelogram (IVP) an x-ray
picture of the kidneys and ureters after
injection of a radiopaque dye; used to locate
kidney stones and to determine the anatomy
of the kidney
o Voiding Cysto-urethrogram (VCUG) - a
minimally invasive test that uses a special x-
ray technology called fluoroscopy to evaluate a
child's bladder size, shape, and capacity, as
well as the urethra. This procedure can also
determine if a child has reflux a condition
where urine from the bladder goes upward
back to the kidneys. This exam may be
ordered after a child experiences frequent
urinary tract infections.
Vascular Imaging
o Angiogram
o Echoangiogram
Scan
o Technetium Scan
o CT-Scan anatomic
o Magnetic Resonance Imaging (MRI)
vascular and anatomic

BLOOD TESTS
Complete Blood Count, Hemoglobin, Hematocrit,
WBC, RBC, platelets, Bilirubin
Chemical
Blood Urea Nitrogen (BUN), Creatinine
Electrolytes
Protein, sugar
Hemolytic products to diagnose Hemolytic
Uremic Syndrome
Immunologic Products - e.g.to diagnose IgA
nephropathy,
Systemic markers Anti-neutrophil cytoplasmic
antibody (ANCA), Anti-neutrophilic antibodies (ANA);
useful for diagnosis of glomerulonephritis

HISTOLOGY
Light Microscopy
Electron Microscopy
Micropuncture Functional Studies

CLINICAL DISEASES IN CHILDREN
URINARY TRACT INFECTION
Urethra and Bladder
Ascending peri-anal and intestinal bacteria
no. 1 cause is E. coli
Fungal

Common age group: 3 y/o and below. (Can be Up to
5 y/o)
In girls, the first UTI usually occurs by the age of 5 yr,
with peaksduring infancy and toilet training
In boys, most UTIs occur during the 1st yr of life
UTIs are caused mainly by colonic bacteria
In girls, 75-90% of all infections are caused by
Escherichia coli,followed byKlebsiellaspp and Proteus
spp
Usually manifests as Proteinuria + Pus in urine
Upon urination bacteria will stick to urethra
migrateupwards causing CYSTITIS (inflammation of
bladder wall) when bladder contracts, there is pain
irritable muscles, nerveendings epithelium is affected
dysuria
Cystitis indicates that there is bladder involvement.
Symptoms include dysuria, urgency, frequency,
suprapubicpain, incontinence, and malodorous urine.
Cystitis does not cause fever and does not result in
renal injury
Recurrent UTI- common cause of Rena Failure
During infancy, valve effect of ureterovesical junction is
still very weakpredisposing them to vesicoureteral
reflux
When there is predominant WBCs and proteinuria in
urinalyis, plus fever it is best to presume that this
ispyelonephritis rather than just simple lower
UTIaggressive treatment needed to protect kidneys
and prevent renal insufficiency.
The 3 basic forms of UTI:
Pyelonephritis
Cystitis
Asymptomatic bacteriuria

SIGNS AND SYMPTOMS OF UTI
A. LOWER URINARY TRACT INFECTION
Dysuria
Frequency/ small amounts
Non-specific discomfort
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Fever is infrequent (but may be positive)

B. UPPER URINARY TRACT
INFECTION/PYELONEPHRITIS
Fever and systemic signs patient becomes highly
febrile because toxins and antigens go to the highly
vascular kidneys; pag highly febrile ang patient, usually
Upper Urinary Tract ang involved; High fever also
denotes a more serious infection
Flank pain
Non-specific signs of serious illness

DIAGNOSIS
A. DIRECT (localized)
Urinalysis
Shows Increased WBC (>5/hpf)
+/- RBCs
Pyuria (leukocytes in urine) suggests infection, but
infection can occur in the absence of ofpyuria; this
finding is more confirmatory than diagnostic.
Conversely, pyuria can be present without UTI.
Urine Culture/Sensitivity
Usually reveals E. coli
Usually 100,000 (10
5
) CFU but may also be 10
4

or 10
3
because frequent urination may provide less
time for bacteria to grow, thus less bacteria are
detected in Urine C/S
Child who is sick with 100,000 colonies definitely
UTI but should present with pus cells in urinalysis
o 10,000 colonies + symptoms diagnose as UTI
o 1,000 colonies + symptoms diagnose as UTI

B. SYSTEMIC
CBC Increased WBC, Anemia in chronic disease
Blood C/S
Creatinine measures excretion function
In children: Normal Creatinine = 0.4-0.8
mg/dL
In adults: Normal Creatinine = 1-1.5 mg/dL

C. ANATOMIC IMAGING
Ultrasound more useful for Upper UTI
Bladder thickened, irregular
Ureters visible, wide and with abnormal contour
Kidneys enlarged in UTI, small in chronic cases
due to scar formation wherein dead nephrons are
replaced by non-functional scar tissues
X-ray allows visualization of stones
Technetium
To visualize scars
Shows delayed opacification
Shows delayed excretion
Shows contracted or enlarged kidneys

TREATMENT
Empiric
Ampicillin
Co-amoxiclav + Aminoglycoside
Parenteral antibiotics expect improvement after 3
days. If urinalysis appears to be normal already,
patient may shift to oral antibiotics to complete the
recommended 7-day regimen.
Based on Culture and Sensitivity Results takes 48
to 72 hours, so empiric treatment may be given first. If
the patient shows to be sensitive to the empiric
treatment given and has a good response then the
antibiotic may be continued. If (-) sensitivity but (+)
good responses, its up to the physician to decide
whether to change the antibiotic or not.
Follow-up Treatment
Urinalysis to see if the urine has improved or if
the patient is responding well to treatment
Culture and Sensitivity - sometimes done to
know if there is still some bacteria left
Follow-up imaging changes in the kidney may
be seen after 6 months to 1 year. e.g. scar
formation will not become normal until 6 months to
1 year

VESICO-URETERAL REFLUX

NORMAL URINARY TRACT
Vesicoureteric junction does not allow retrograde
flow of urine from bladder to the kidney

VESICOURETERAL REFLEX
Phenomenon of backward-upward flow of urine
Permit transport of urine from bladder to the kidney
May be uni-/bilateral
Demonstrated and grade by Voiding
Cystourethrogram

PATHOPHYSIOLOGY
Bacterial invasion and multiplication Inflammation
and host reaction Loss of normal renal function
Necrosis of renal tissue
Aggressive treatment is done to avoid destruction of
the area

1. BACTERIAL INVASION AND MULTIPLICATION
Bacteria from stools
Proximity of urethra
Adherence of E. coli that resists urine flow
Ascends from urethra to bladder (cystitis, lower UTI)
Ascends from bladder to ureters (reflux)
Ascends from ureters to kidney (pyelonephritis)
Low to negative bacterial growth by culture and
sensitivity
Short bladder time = newborn and infants
Low dose antibiotics
Wrong culture and media used

2. INFLAMMATION AND HOST REACTION
Bladder irritation
o Hypercontracted bladder wall frequent small
amount of urine
To diagnose bladder function, UTZ shows bladder
walls thicker than normal
Inflammation edemathickening of walls
Increased WBC during inflammation
Diluted urine due to failure to concentrate
Glomerulus is not affected so filtration is not
affected
Creatinine clearance for kidney function test
Kinds:
a. Urethritis
o Dysuria, burning sensation
b. Cystitis
o Dysuria, bladder tenderness, frequent urination
with fever
o On UTZ: thickened bladder wall
c. Pyelonephritis
o Systemic symptoms

3. LOSS OF RENAL FUNCTION
Decreased number of nephrons
Nephron hypertrophy early aging
hyperfiltrationnephrosclerosisdestruction
(proteinuria and HTN) renal insufficiency renal
failure

4. NECROSIS OF RENAL PARENCHYMA
Tubule and surrounding intersitium are inflamed
Destruction of growth of functional cells (growth
factors, vit D, erythropoietin, prostaglandins,
hormones)
Tubule destroyed, glomerulus obliterates
Area replaced by non-functional scar tissue
Number of nephrons are reduced
Remaining nephrons are overworked
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REFLUX GRADING

Figure 2. Reflux grading (Nelson)

Table 3.Reflux Grading
GRADE DESCRIPTION
Grade 1 Reflux into a nondilated ureter
Grade 2 Reflux into the upper collecting system
without dilation
Grade 3 Reflux into a dilated ureter and/or
blunting of calycealfornices
Grade 4 Reflux into a grossly dilated ureter
Grade 5 Massive Reflux with significant
dilatation and tortuosity and loss of
capillary impression

WHAT TO DO WITH PYELONEPHRITIS:
VESICOURETERAL REFLUX
1. Prophylactic Antibiotic continuous prophylactic
low dose single daily antibiotic. Advise to take nightly
so in the morning, the patient will urinate. So there is
a long period of time for antibiotics to stay in the
body. However, this is only effective in older children
and adults because infants urinate every 2 hours.
Ditopapasokyungsinabini doc na choice of antibiotic. It
may either be
a. 500 mg penicillin it is very effective but after 4
hours it will already be excreted leaving the
urinary tract vulnerable for infection again
b. Cotrimoxazole after 12 hours (6 to 8 hours sa
past trans), drug will concentrate in the kidneys. If
the patient sleeps (without urinating) and urine
refluxes, he/she is protected because the antibiotic
is still present. Cotrimoxazole is the one used in
adults or older children
2. Reflux repair by re-implantation of ureter by urologist
3. Periodic urinalysis/ Culture and sensitivity to
document recurrent UTI must be done especially
if patient experiences recurrent UTI as this poses a
higher risk for vesico-ureteral refulx
4. Health status monitoring
a. Renal function
b. Anthropometric evaluation
5. Follow-up imaging
a. For anatomic changes scar formation
b. For determination of functional status
6. Blood tests for evaluation of renal function

POST-INFECTIOUS ACUTE
GLOMERULONEPHRITIS/ POST-STREPTOCOCCAL
ACUTE GLOMERULONEPHRITIS (PSAGN)
The usual age group affected: 4-9 years old
Accdg to Nelsons, PSGN most common in children aged
5-12 yr and uncommon before the age of 3 yr.
4 features of AGN
Edema
Oliguria
HPN
Hematuria
Depending on the severity of renal involvement,
patients can develop various degrees of edema,
hypertension, and oliguria.
Nonspecific symptoms such as malaise, lethargy,
abdominal pain, or flank pain are common.
AGN is not an infection but an immunologic disease
depression in the serum complement (C3) level
provide strong evidence that ASPGN is mediated by
immune complexes
Occurs AFTER strep infection PSAGN
Group A -hemolytic streptococcal
(GABHS)infections are common in children and can
lead to the postinfectious complication of acute
glomerulonephritis (GN)
The usual infection is not sore throat.
In rheumatic fever, it is usually sore throat.
In PSGN, it is usually streptococcal skin infection.
The typical patient develops an acute nephritic
syndrome 1-2 wk after an antecedent streptococcal
pharyngitis or 3-6 wk after a streptococcal
pyoderma
The history of a specific infection may be absent,
because symptoms may have been mild or have
resolved without patients receiving specific
treatment or seeking the care of a medical provider.
There is predominantly RBC in PSGN
Also presents with proteinuria, but this isnt used as a
criterion.
Sometimes will have small amount of WBC because it is
an inflammatory disease, but more predominant ang
RBC (10-15 WBC, 20 RBC)
Presence of signs of inflammation: edema, swelling,
dysfunction
In PSGN: edema of capillaries spaces becomes small
filtration and excretion of water and solutes become
impairededema, HPN, oliguria, hematuria.
Fluid retentionedema
o Starts perioorbitally, noticeable upon waking up
o Gravitates towards lower extremities on
prolonged standing
o Taut but puts on pressure
Unable to excrete fluids oliguria
o Voids rarely or goes to toilet frequently without
passing out urine
Fluid overload congestion
Will produce some escape of RBCs hematuria
o Varies from microscopic to gross
o Frankly bloody, smoky brown or tea-colored
o Most alarming sign but not an indication for
admission
Fluid overload and congestion hypertension
o Nuchal pain, headache, vomiting, transient
visual loss
o Systolic and diastolic BP levels are generally
above 120/80 mmHg, respectively
o Patients are at risk for developing encephalopathy
and/or heart failure secondary to hypertension or
hypervolemia.
o Hypertensive encephalopathy must be considered
in patients with blurred vision, severe headaches,
altered mental status, or new seizures
Hematuria is not an indication for admission. Usually
they are admitted due to edema or congestion or
problematic blood pressure

Table 4. Comparison between UTI and PSAGN
UTI PSAGN
Increased WBC shown in
urinalysis
Increased RBC

Usually involves tubules,
interstitium
Involves the glomerulus
+ Protein + Protein, small
amounts
Sepsis and Scar Good recovery in 6 to 8
weeks
Normal volume of urine
and pyuria
May involve Oliguria







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Figure 3.Clinical Course of PSAGN

Typical course lasts for 7 to 10 days for each of the
three phases:

1.Oliguric Phase
o Acute salt and water overload
o Complications: hypertensive encephalopathy,
renal failure, CHF
o Phase shortened by the use of parenteral
diuretics
2.Diuretic Phase (3-5 days)
o Levelling of the daily weight curve, then
spontaneous voiding or sudden volume
increments with diuretic agents
o BP normalizes and the child starts feeling better
3.Immediate Convalescent
o Most hospitalized children are ready for discharge
o All alarming indices in the oliguric period are gone
except for residual gross or significant
microscopic hematuria.

DIAGNOSIS/FEATURES OF GLOMERULAR
DISEASES
A. Urinalysis
Gross (macroscopic) hematuria
Normal to high specific gravity
Mild to absent WBC
RBC casts
protein
B. Blood tests
CBC = normal or with slight anemia
Serum protein (albumin) = normal
BUN, Creatinine = Normal or <10% azotemia
electrolytes
C3 = low
C. Imaging
Normal to enlarged kidney
Screen to rule out systemic disease like SLE or HSP
Acute Glomerulonephritis should subsidein 8 weeks
to 1 year
o If it recurs after 8 weeks, it is now considered as
chronic renal disease or chronic
glomerulonephritis
o No recurrence after 6 months to 1 year means
good prognosis
D. Biopsy
1-5% progress to RPGN
Recurrence of signs and symptoms implies non-post
infection streptococcal AGN
Biopsy indicated if signs and symptoms persist
with atypical presentation
Not indicated with improvement of signs and
symptoms
Remember that PSAGN usually does not recur
E. Anti-streptolysin O titer (ASO titer)
usually negative
F. Anti-DNAse titer
Positive in post-skin infection but not during the
infection

TREATMENT
Hematuria is not an indication for hospital admission;
no treatment for this; furthermore, anemia from
hematuria is INSIGNIFICANT
Oliguria and edema are indications for admission as
they may lead to complications such as CHF,
hypertensive encephalopathy, etc.
Water and salt restriction. Limit to 3 mg/kg/day
Sodium intake
Diuretics like Furosemide
Hypertension is due to water restriction
Water and salt restriction
Antihypertensives/diuretics like Furosemide
Post-streptococcal infection
May be treated with Penicillin to eliminate any
residual carrier state for Streptococcus which may
be infect other people

NEPHROTIC SYNDROME
(MINIMAL CHANGE DISEASE)
Age incidence: 1-3 yrs old onset
Minimal change glomerular histopathologic disease (or
no change that can be seen by light microscopy)
Electron microscopy
Basement membrane immune deposits
Selective albuminuria (proteinuria) passage of
albumin to the basement membrane
Massive albuminuria greater than 1 g/m
2
/24
hours (>40mg/m
2
/hour)
Edema
Massive proteinuria
Hypoalbuminemia
Hyperlipidemia usually present, but not necessary
to diagnose the disease because if you already have
massive proteinuria, then it is already diagnosed as
NS
Hypotension
Postural hypotension (orthostatic)
No hematuria, no pyuria
In nephrotic syndrome, the presentation are edema
which may have normal BP or hypotension (unlike
glomerulonephritis which has hypertension as
manifestation)
Nephrotic syndrome is not just proteinuria, it is
massive proteinuria compared to other proteinuric
states of other disease
There is also hypovolemia in NS due to loss of
albumin in the urine
90% of NS that presents with edema, massive
proteinuria and hypoalbuminemia typically will have
hematuria
Usually associated with hypocalcemia because
calcium are mostly albumin-bound, thus when you lose
albumin, you also lose calcium

DIAGNOSTIC TESTS
Urinalysis
+3 to +4 proteinuria
No or transient mild hematuria/pyuria(but not part
of diagnostic criteria)
No evidence of infection

Hematuria
Oliguria
Edema
Hypertension
Gross to microscopic
hematuria (minus
edema and
hypertension
Microscopic
hematuria
Variants:
1. Chronic
glomerulonephritis
2. Rapidly progressive
glomerulonephritis
(RPGN)
Acute Stage =
7-14 days
Diuretic Stage
Recovery or
Convalescent
Stage
Complete
Recovery:
8 weeks average
(6 mos to 1
year)
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Systemic
CBC normal (sometimes elevated platelet count)
BUN, Creatinine normal
C3 normal
Hyperlipidemia
Hypoalbuminemialess than 25 g/dl
Hypercoagulability(prone to thrombosis)
o Blood volume is decreased, concentrated blood
products.
o Aside from albumin, glomeruli are also excreting
the blood products of anticoagulation thus the
hypercoagulability
o Thus, you see to it that the blood extractions in
these patients are atraumatic to prevent
thrombosis
Anatomic Imaging normal
Biopsy is not usually required but is indicated if there
is:
Steroid resistance
Initial response followed by 2x resistance
Late age onset (12 years old and higher) usually
steroid resistance

TREATMENT
Prednisone
60 mg/m
2
/day 4-6 weeks (divided into 3 doses;
after meal)
o You do not have to taper the dose until the 4
th
-6
th

week to prevent relapse of proteinuria
Taper the dose to 40 mg/m
2
/day(single dose in
the morning) you give this every other day for
another 4-8 weeks
Prophylactic anti-TB (Isoniazid) in the
Philippines, you do this because of the endemicity of
TB in the country
When the patient becomes negative and no edema,
the recurrence is usually induced by infections,
usually upper respiratory tract infections in
childhood
o In case of recurrence, you treat the infection,
and resume Prednisone 60 mg/m
2
/day. You
may do it shorter or 4-6 weeks as long as the
proteinuria has been negative for 3-5 consecutive
weeks.
Good prognosis in 1-3 years old good response
with steroids
Good prognosis if it is the classical presentation of NS
DO NOT TREAT THE EDEMA OF NS WITH
DIURETICS dangerous, worsens hypovolemia
May cause acute renal injury or significant oliguria
because you are depleting further the blood volume

OTHER VARIETIES OF NS
Focal segmental glomerulosclerosis (FSGS) IgA
Nephropathy
Membranous glomerulonephritis
Progressive nephritis of systemic immunological disease
(eg.SLE, HSP)

PROGRESSIVE RENAL DISEASE
Characterized by continuous deterioration of renal
function
Reduction of nephrons
Reduction of renal tissue (scarring) replacement by
non-functional scars
Progression to azotemia
Anemia associated with decrease in erythropoietin
Growth and functional impairment
Uremic disease
Renal failure
Electrolyte abnormalities
No renal regeneration
Metabolic acidosis/alkalosis but usually acidosis


ACUTE RENAL FAILURE (AKI/ARF)
Azotemia and oliguria usual manifestation of ARF
But there is also non-oliguric ARF but with azotemia
Inflammation of glomerulus proliferation of
mesangial cells decrease filtration due to
overcrowding of mesangial cells oliguria
Excretion of metabolic products azotemia
Cardiovascular causes:
Hypovolemic dehydration
Acute cardiac failure
Vascular disease
o Large to small vascular diseases
o Microvasculitis
Systemic Lupus Erythematosus (SLE)
Kawasaki
HenochSchonleinPurpura (HSP)
Triad: purpura, abdominal pain, renal
insufficiency
Also has arthritis or joint pain
Hemolytic Uremic Syndrome (HUS)
Mild to moderate diarrhea
Anemia
Oliguria
Acidosis
Convulsion
Due to infection like e. coli
Toxins will cause vasoconstriction of renal
vasculature clumping of platelets and
turbulence of flow hemolysis
Renovascular thrombosis (Renal Vein Thrombosis)
Sepsis
Prematurity
Toxins
Renal tubular injuries
o Example: Tumor lysis causes hyperuricemia or
increase uric acid which is toxic to the tubular
epithelium
o Massive injury like crush syndrome muscular
destruction myoglobinuria (myoglobin is toxic
to tubular epithelium)
o Some drugs

THERAPEUTIC CONSIDERATIONS
Associated symptoms with the antecedent cause
May improve with withdrawal of the cause
Need for supportive treatment
Rehydration (1
st
72 hours)
Nutrition
Electrolyte correction
Correction of acidosis/alkalosis
Renal replacement therapy
Dialysis
In children, it is not easy to do hemodialysis, thus
peritoneal dialysis is preferred

RENAL TUBULAR DISEASES
Renal Tubular Acidosis acidosis
Means tubules are losing a lot of bicarbonates
Bartters Syndrome and Gittlmans Syndrome
alkalosis
A lot of acids are lost
Associated with failure to thrive, dehydration, and
hypokalemia
Fanconis syndrome total tubular dysfunction
Inability to absorb everything including sugar and
protein
Pan-tubular dysfunction








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OTHER NOTES
Normal:

Figure 4: Normal

In diarrhea, loss of bicarbonate acidosis
Urine is acidic because dun motinataponang acids sa
urine due to metabolic acidosis
If normal ang anion gap or no change in the level of
the other anions, then the chloride ions will increase
resulting to hyperchloremic metabolic acidosis.
In non-diarrheal state but loss of bicarbonate then
the loss may be due in the urine (thus alkaloticyung
urine mo) also hyperchloremic metabolic acidosis
If there is loss of bicarbonate but with normal anion
gap, then you will have hyperchloremic acidosis
(kasiyung chlorine angtataas to maintain the balance)


Figure 5: Hyperchloremic Metabolic Acidosis























In sepsis:
Increased production of lactic acid increase yung
other anions mo so the bicarbonate will decrease
Hypo-anion gap metabolic acidosis (though di
komagets kung bakit hypo, bastayunangsabini doc)

Figure 6: Hypo-anion gap metabolic acidosis

Diabetic ketoacidosis:
Increase acid as ketone
High increase anion gap metabolic acidosis (di
komagets kung bakitbastayansabini doc. Hehe)
Vomiting
Loss of chloride increase bicarbonate alkalosis
Hypochloremic metabolic alkalosis (also can be
caused by loss of chloride ions in the urine due to
poor reabsorption in the kidney)

Figure 7:Hypochloremic metabolic alkalosis

In normal anion gap, ang gagalaw lang ay ang
bicarbonate and chloride ions. Normal means walang
increase in other anions such as lactates, phosphates,
sulfates, etc.
In either alkalosis or acidosis, you will have
dehydration because you are losing a lot of
electrolytes (osmotic diuresis). You also lose
potassium thus you will have hypokalemia manifested
by weakness.