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Insuficienta renala

 Rinichii asigura trei functii majore:
- filtrarea sangelui si producerea
urinei pentru eliminarea deseurilor,
impiedicand astfel acumularea
toxinelor in sange
- reglarea concentratiei mineralelor si
electrolitilor (sodiu, calciu si potasiu)
si cantitatea de lichid din organism
- producerea de hormoni care
actioneaza asupra altor functii ale
corpului, precum reglarea tensiunii
arteriale (renina) si producerea de
globule rosii (eritropoietina).
 Insuficienta renala cronica (IRC)
reprezinta diminuarea lenta si
progresiva a capacitatii de filtrare a
 IRC survine de obicei drept
complicatie a altei boli sau afectiuni.
 Spre deosebire de insuficienta renala
acuta, IRC se instaleaza progresiv, pe
parcursul mai multor ani, pe masura
deteriorarii rinichilor.
 Evolutia este atat de lenta, incat
primele simptome apar doar dupa ce
boala a determinat consecinte clinice
 Insuficienta renala cronica reprezinta
etapa finala a bolilor renale
bilaterale, în special a
glomerulonefritelor cronice, a
glomerulonefrozelor si a
pielonefritelor cronice, a
hipertensiunii arteriale maligne, a
obstructiilor cailor urinare.
 în mod normal rinichiul are o rezerva
functionala care-i permite sa se
adapteze unor solicitari crescute.
 în insuficienta renala, distrugerea
nefronilor nu mai permite aceasta
 Prima functie alterata este
capacitatea de concentratie. în
stadiul initial, rinichiul poate asigura
homeostazia mediului intern, adica
sa mentina constanta cantitatea de
sare, apa, substante azotate si
electroliti din organism, ceea ce se
realizeaza prin unele mecanisme
 In aceasta perioada, poliuria se însoteste
de hipostenurie, deci de scaderea
capacitatii de concentratie.
 Odata cu progresarea leziunilor, poliuria
devine maxima si scaderea capacitatii de
concentratie este foarte severa. Aceasta
este faza de izostenurie, când densitatea
urinii oscileaza invariabil între 1 010 si 1
 în ultimul stadiu, insuficienta renala se
decompenseaza si apare uremia.
 chronic kidney disease as either
kidney damage or a decreased
kidney glomerular filtration rate
(GFR) of less than 60 mL/min/1.73
m2 for 3 or more months.
 Whatever the underlying etiology,
the destruction of renal mass with
irreversible sclerosis and loss of
nephrons leads to a progressive
decline in GFR.
 Stage 1: Kidney damage with normal
or increased GFR (>90 mL/min/1.73
 Stage 2: Mild reduction in GFR (60-89
mL/min/1.73 m2)
 Stage 3: Moderate reduction in GFR
(30-59 mL/min/1.73 m2)
 Stage 4: Severe reduction in GFR (15-
29 mL/min/1.73 m2)
 Stage 5: Kidney failure (GFR <15
mL/min/1.73 m2 or dialysis)
 Approximately 1 million nephrons are
present in each kidney, each
contributing to the total GFR.
Regardless of the etiology of renal
injury, with progressive destruction
of nephrons, the kidney has an
innate ability to maintain GFR by
hyperfiltration and compensatory
hypertrophy of the remaining healthy
 This nephron adaptability allows for
continued normal clearance of plasma
solutes so that substances such as urea
and creatinine start to show significant
increases in plasma levels only after total
GFR has decreased to 50%, when the renal
reserve has been exhausted. The plasma
creatinine value will approximately double
with a 50% reduction in GFR. A rise in
plasma creatinine from a baseline value of
0.6 mg/dL to 1.2 mg/dL in a patient,
although still within the reference range,
actually represents a loss of 50% of
 The residual nephron hyperfiltration and
hypertrophy, although beneficial for the
reasons noted, has been hypothesized to
represent a major cause of progressive
renal dysfunction. This is believed to occur
because of increased glomerular capillary
pressure, which damages the capillaries
and leads initially to focal and segmental
glomerulosclerosis and eventually to
global glomerulosclerosis. This hypothesis
has been based on studies of five-sixths
nephrectomized rats, which
develop lesions that are identical to those
 Factors other than the underlying disease process
and glomerular hypertension that may cause
progressive renal injury include the following:
 Systemic hypertension
 Acute insults from nephrotoxins or
decreased perfusion
 Proteinuria
 Increased renal ammoniagenesis with
interstitial injury
 Hyperlipidemia
 Hyperphosphatemia with calcium phosphate
 Decreased levels of nitrous oxide
 Smoking
 CKD can be roughly categorized as
diminished renal reserve, renal
insufficiency, or renal failure (end-
stage renal disease). Initially, as
renal tissue loses function, there are
few abnormalities because the
remaining tissue increases its
performance (renal functional
adaptation); a loss of 75% of renal
tissue produces a fall in GFR to only
 Decreased renal function interferes
with the kidneys' ability to maintain
fluid and electrolyte homeostasis.
Changes proceed predictably, but
considerable overlap and individual
variation exist. The ability to
concentrate urine declines early and
is followed by decreases in ability to
excrete phosphate, acid, and K.
When renal failure is advanced (GFR
≤ 10 mL/min/1.73 m2), the ability to
dilute urine is lost; thus urine
osmolality is usually fixed close to
that of plasma (300 to 320
mOsm/kg), and urinary volume does
 Plasma concentrations of creatinine
and urea (which are highly
dependent on glomerular filtration)
begin a nonlinear rise as GFR
diminishes. These changes are
minimal early on. When the GFR falls
below 10 mL/min/1.73 m2 (normal =
100 mL/min/1.73 m2), their levels
increase rapidly and are usually
associated with systemic
manifestations (uremia). Urea and
creatinine are not major contributors
to the uremic symptoms; they are
markers for many other substances
 Despite a diminishing GFR, Na and
water balance is well maintained by
increased fractional excretion of Na
and a normal response to thirst.
Thus, the plasma Na concentration is
typically normal, and hypervolemia is
infrequent unless dietary intake of
Na or water is very restricted or
excessive. Heart failure can occur
from Na and water overload,
particularly in patients with
decreased cardiac reserve.
 Chronic renal failure (CRF) is the
progressive loss of kidney function.
The kidneys attempt to compensate
for renal damage by hyperfiltration
(excessive straining of the blood)
within the remaining functional
nephrons (filtering units that consist
of a glomerulus and corresponding
tubule). Over time, hyperfiltration
causes further loss of function.
 Chronic loss of function causes
generalized wasting (shrinking in
size) and progressive scarring within
all parts of the kidneys. In time,
overall scarring obscures the site of
the initial damage. Yet, it is not until
over 70% of the normal combined
function of both kidneys is lost that
most patients begin to experience
symptoms of kidney failure.
Chronic renal failure (CRF) can be
classified by the site (location) of
primary damage:
 Pre-renal CRF

 Post-renal CRF (obstructive uropathy)

 Renal CRF
 The cause for CRF sometimes can be
determined by a detailed medical
history, a comprehensive physical
examination, and laboratory studies.
 Even a kidney biopsy may be
inconclusive, because all forms of
kidney failure eventually progress to
diffuse scarring and look the same on
kidney biopsy.
 The most common causes for CRF
are diabetes and high blood
pressure (hypertension.)
Pre-Renal CRF
 Some medical conditions cause
continuous hypoperfusion (low blood
flow) of the kidneys, leading to
kidney atrophy (shrinking), loss of
nephron function, and chronic renal
failure (CRF).
 These conditions include poor cardiac
function, chronic liver failure, and
atherosclerosis ("hardening") of the
renal arteries.
 Each of these conditions can induce
ischemic nephropathy.
Post-Renal CRF
Interference with the normal flow of urine can
produce backpressure within the kidneys, can
damage nephrons, and lead to obstructive
uropathy, a disease of the urinary tract. Bladder
outlet obstruction due to an enlarged prostate
gland or bladder stone
 Neurogenic bladder, an overdistended bladder
caused by impaired communicator nerve fibers
from the bladder to the spinal cord
 Kidney stones in both ureters, the tubes that
pass urine from each kidney to the bladder
 Obstruction of the tubules,the end channels of
the renal nephrons
 Retroperitoneal fibrosis, the formation of
fiberlike tissue behind the peritoneum, the
membrane that lines the abdominal cavity
 Vesicoureteral reflux (VUR), the backward flow
of urine from the bladder into a ureter
Renal CRF
Chronic renal failure caused by changes within
the kidneys, is called renal CRF, and is broadly
categorized as follows:
 Diabetic nephropathy, kidney disease
associated with diabetes; the most common
cause of CRF
 Hypertension nephrosclerosis, a condition
that occurs with increased frequency in African
Americans; the second leading cause of CRF
 Chronic glomerular nephritis, a condition
caused by diseases that affect the glomeruli and
bring about progressive dysfunction
 Chronic interstitial nephritis, a condition
caused by disorders that ultimately lead to
progressive scarring of the interstitium
 Renal vascular CRF, large vessel abnormalities
such as renal artery stenosis (narrowing of the
Signs and Symptoms

 Chronic renal failure (CRF) usually

produces symptoms when renal
function — which is measured as the
glomerular filtration rate (GFR) —
falls below 30 milliliters per minute
(< 30 mL/min). This is approximately
30% of the normal value.
Uremic symptoms can affect every organ system,
most noticeably the following:
 Neurological system–cognitive impairment,
personality change, asterixis (motor disturbance
that affects groups of muscles), seizures (rare)
 Gastrointestinal system–nausea, vomiting,
food distaste (often described as bland, metallic,
"like cardboard")
 Blood-forming system–anemia due to
erythropoetin deficiency, easy bruising and
bleeding due to abnormal platelets
 Pulmonary system–fluid in the lungs, with
breathing difficulties
 Cardiovascular system –chest pain due to
inflammation of the sac surrounding the heart
(pericarditis) and pericardial effusion (fluid
accumulation around the heart)
 Skin –generalized itching
 Chronic renal failure (CRF) is diagnosed by
the observation of a combination of
symptoms and elevated blood urea
nitrogen (BUN) and creatinine (Cr) levels.
The following abnormalities found in the
blood may signal CRF:
 Anemia (low red blood cell count)
 High level of parathyroid hormone
 Hypocalcemia (low blood level of calcium)
 Hyperphosphatemia (high blood level of
 Hyperkalemia (high blood level of
 Hyponatremia (low blood level of sodium)
 Low blood level of bicarbonate
 With the loss of kidney function,
phosphate accumulates in the blood.
 Excess phosphate in the blood reduces
levels of blood calcium, and low blood
calcium levels trigger the parathyroid
gland (located in the neck) to release
more parathyroid hormone (PTH).
 PTH then dissolves bone tissue to release
stored calcium and raise the level of
calcium in the blood. This chronic cycle of
events is called secondary
 The net result of this condition is the
development of metabolic bone disease
(renal osteodystrophy). These patients are
at risk for bone fractures, bone and muscle
Acute renal failure (ARF)

 is the rapid breakdown of renal

(kidney) function that occurs when
high levels of uremic toxins (waste
products of the body's metabolism)
accumulate in the blood.
 ARF occurs when the kidneys are
unable to excrete (discharge) the
daily load of toxins in the urine.
Based on the amount of urine that is
excreted over a 24-hour period,
patients with ARF are separated into
two groups:
 Oliguric: patients who excrete less
than 500 milliliters per day (< 16
 Nonoliguric: patients who excrete
more than 500 milliliters per day (>
16 oz/day)
In nonoliguric patients, the urine is of
poor quality (i.e., contains little
waste) because the blood is not well
 Both kidneys are failing when ARF
occurs. One normally functioning
kidney can maintain adequate blood
The three types of ARF are named for
their location within the renal
(kidney) system:

 Prerenal ARF
 Postrenal ARF
 Intrinsic renal ARF
Prerenal Acute Renal Failure (ARF)
 Some of the most notable causes of prerenal ARF
are dehydration, heart failure, sepsis (severe
infection), and severe blood loss.
 Prerenal ARF is associated with a number of
preexisting medical conditions, such as
atherosclerosis ("hardening" of the arteries with
fatty deposits), which reduces blood flow.
 Dehydration caused by drastically reduced fluid
intake or excessive use of diuretics (water pills) is
a major cause of prerenal ARF. Many people with
severe heart conditions are kept slightly
dehydrated by the diuretics they take to prevent
fluid buildup in their lungs, and they often have
reduced blood flow (underperfusion) to the
 Risk Factors
 Atherosclerosis
 Blood loss
Postrenal Acute Renal Failure (ARF)
 Some of the most notable causes of postrenal
ARF include the following:
 Bladder outlet obstruction due to an enlarged
prostate gland or bladder stone
 Kidney stones in both ureters (tubes that pass
urine from each kidney to the bladder) or in
patients with one kidney
 Neurogenic bladder (overdistended bladder
caused by inability of the bladder to empty)
 Tubule obstruction (end channels of the renal
 Renal injury (usually sustained in an automobile
accident or while playing a sport)
 Retroperitoneal fibrosis (formation of fibrous
tissue behind the peritoneum—the membrane
that lines the abdominal cavity)
Intrinsic Acute Renal Failure (ARF)
 The causes can be classified as follows:
 Vascular disease
 Glomerulonephritis (GN) and vasculitis
(inflammation of blood vessels)
 Renal artery obstruction (atherosclerosis,
 Renal vein obstruction (thrombosis)
 TTP-HUS (low blood platelet and red blood cell
 Diseases of tubules and interstitium
(space between parts of tissue)
 Amyloidosis (deposition of proteins in kidney
 Interstitial nephritis (associated with allergy or
 Acute tubular necrosis

 Intrinsic ARF accounts for approximately
40% of the cases of acute renal failure.
 Nearly 90% of intrinsic ARF cases are
caused by ischemia or toxins, both of
which lead to acute tubular necrosis (ATN).
Ischemic ARF is associated with reduced
blood flow to the kidneys (renal
hypoperfusion), which leads to tissue
death and irreversible kidney failure.
Ischemic ARF occurs most frequently when
there is hemorrhage (blood loss), trauma,
or sepsis (severe infection), and in patients
undergoing major cardiovascular surgery.
 Many types of medication can cause
nephrotoxic intrinsic ARF, and the effect
seems to be dose related. Most cases
occur in the elderly and in patients with
chronic renal failure (CRF). Toxins taken
into the body that can trigger intrinsic ARF
include the following:
 Antibiotics (e.g., acyclovir, roscarnet)
 Chemotherapeutic drugs (used to treat
cancer, e.g., cisplatin, ifosfamide)
 Cyclosporine
 Radiocontrast dyes (used in imaging
 Some toxins are released by tissues as a
result of injury or are created by
electrolyte imbalance. Some endogenous
toxins that trigger nephrotoxic ARF include
the following:
 Rhabdomyolysis (release of myoglobin in
the urine resulting from the destruction of
muscle tissue) caused by the following:
 Intoxication (e.g., alcohol, cocaine)
 Seizure
 Traumatic crush injury
 Hypercalcemia (high level of calcium in
the blood) caused by the following:
 Deposition of calcium in tissue
 Vasoconstriction (reduced diameter of blood
 Both ischemic and nephrotoxic ARF
cause acute tubular necrosis (ATN),
but ATN is less pronounced in
nephrotoxic ARF.
 Allergic interstitial nephritis can be
triggered by several different types
of drugs. The most common are:
 antibiotics (e.g., penicillin,
cephalosporins) and
 nonsteroidal anti-inflammatory drugs
(e.g., acetaminophen, ibuprofen).
Signs and Symptoms
 Fever, rash, arthralgia (joint pain)—
associated with allergic interstitial
 Flank pain—associated with renal
artery or vein obstruction, severe
 Headache, dizziness, confusion,
seizure—associated with malignant
 Oliguria (reduced urination), edema
(swelling), hypertension—associated
with glomerulonephritis, vasculitis
 Papilledema (swollen optic disk),
Because excretion of sodium and
potassium is impaired, levels of these
minerals and the level of chloride in the
blood become elevated. This condition is
known as metabolic acidosis. Several
other complications may occur during the
course of intrinsic ARF, including the
 Hyperkalemia (high level of potassium in
the blood)
 Hypermagnamesia (high level of
magnesium in the blood)
 Hyperphosphatemia (high level of
phosphates in the blood)
 Hypocalcemia (low level of calcium in the
 Intravascular overload (excess fluid in the
 Diagnosis is based on results from blood
tests and urinalysis, and on the patient's
medical history and signs and symptoms.
 Blood test results that show high levels
of creatinine indicate renal ischemia,
atheroembolism, or exposure to
radiocontrast dye. Severe anemia (low red
blood count) may indicate TTP-HUS.
Hyperkalemia (high level of potassium),
hyperphosphatemia (high level of
phosphorous), and hypocalcemia (low
level of calcium) occur in rhabdomyolysis.
 Urinalysis shows many red and white cells
in the urine, and the level of sodium may
be high. Proteinuria is a common finding.
Mild proteinuria suggests that failure is
caused by injured tubules. Moderate
 Before the development of renal
replacement therapy (RRT), many people
with ARF died from severe electrolyte
imbalance (hyperkalemia, acidosis) or
from the uremic toxins themselves.
 Patients with ARF are at risk for numerous
complications that may lead to death,
such as seizures, bleeding, and coma.
Since dialysis effectively treats the life-
threatening complications of ARF,
advanced age and underlying diseases are
more likely to determine the risk for a
 Oliguric ARF patients continue to
have a high mortality rate, despite
the availability of RRT. Almost
uniformly, these patients have other
acute and/or chronic medical
 Patients with nonoliguric ARF tend to
have a more favorable prognosis and
are often easier to treat. Nonoliguric
ARF patients often have fewer
systemwide complications because
their condition typically is caused by