Acute Renal Failure

Acute renal failure develops when renal function is diminished to the point where body
fluid homeostasis can no longer be maintained.
Oliguric renal failure --daily urine volume < 400 mL/m2 or 1ml/kg/hour
Nonoliguric renal failure --urine volume may approximate normal eg- aminoglycoside
nephrotoxicity.
Biochemical criteria for RF- blood urea nitrogen [BUN],
Creatinine
urine volume

ETIOLOGY.

Prerenal-- decreased perfusion of the kidneys results in decreased renal function

Renal --direct involvement of the kidneys,
Postrenal is - primarily of obstructive disorders.

PATHOGENESIS.

Prerenal renal failure - decreased renal perfusion - decrease in the total circulating blood
volume. No kidney damage. Diminished intravascular volume Æ fall in cardiac output,
Æ decline in renal cortical blood flow and glomerular filtration rate (GFR). If underlying
cause of the hypoperfusion is reversed, then renal function may return to normal. If
hypoperfusion persists beyond a critical point, then direct renal parenchymal damage may
develop.

Renal causes of acute renal failure -- - rapidly progressive forms of several types of
glomerulonephritis - causes - acute renal failure in older children. Activation of the
coagulation system within the kidneys, resulting in small vessel thrombosis, Æ acute
renal failure. Acute dehydration and the hemolytic-uremic syndrome are the most
common causes of acute renal failure in toddlers.

Acute tubular necrosis is acute renal failure in the absence of arterial or glomerular
lesions. There is necrosis of the tubular cells.
heavy metals, chemicals- tubular cell necrosis, - alterations in intrarenal blood flow,
tubular obstruction, and passive backflow of the glomerular filtrate across injured tubular
cells .

Acute interstitial nephritis is due to hypersensitivity reaction to a therapeutic agent.

Tumors Æ infiltration of the kidneys or by obstruction of the tubules by uric acid crystals

Developmental abnormalities and hereditary nephritis Inability to conserve sodium and

water is common -If oral intake is compromised (vomiting) or extrarenal salt and water
loss develops (diarrhea), leads to intravascular volume contraction and renal failure.

Postrenal causes of acute renal failure Æobstructions of the urinary tract. Ureteral
obstruction must be bilateral to produce renal failure. Dilatation of the upper collecting
system may take several days to develop in acute Ureteral obstruction.
CLINICAL MANIFESTATIONS.

Clinical findings of the renal failure include

pallor (anemia),
diminished urine output,
edema (salt and water overload),
hypertension,
vomiting,
lethargy (uremic encephalopathy).
Complications of acute renal failure CVS, GIT, CNS
CVS --volume overload with heart failure and pulmonary edema,
arrhythmias,
GIT-- gastrointestinal bleeding due to stress ulcers or gastritis,
CNS - seizures, coma, and behavioral changes.

DIAGNOSIS.

Vomiting, diarrhea, and fever suggest dehydration and prerenal azotemia, , hemolytic-
uremic syndrome , renal vein thrombosis.
Antecedent skin or throat infection suggests poststreptococcal glomerulonephritis.
Rash may be found in systemic lupus erythematosus or Henoch-Schönlein purpura.
A history of exposure to chemicals and medications
Flank masses -- renal vein thrombosis, tumors, cystic disease, or obstruction.

Laboratory abnormalities
anemia (with the rare exception of blood loss, the anemia is usually dilutional or
hemolytic, as in lupus, renal vein thrombosis, and the hemolytic-uremic syndrome);
leukopenia (lupus)
thrombocytopenia (lupus, renal vein thrombosis, hemolytic-uremic syndrome);
hyponatremia (dilutional)
Hyperkalemia
Acidosis
elevated serum concentrations of BUN
creatinine
uric acid
phosphate (diminished renal function)
hypocalcemia (hyperphosphatemia).
The serum C3 level may be depressed (poststreptococcal, lupus, or
membranoproliferative glomerulonephritis)
antibodies
streptococcal (poststreptococcal glomerulonephritis),
nuclear (lupus),
neutrophil cytoplasmic antigens (ANCA; Wegener's granulomatosis, microscopic
polyarteritis),
basement membrane (Goodpasture disease) antigens.
Chest roentgenography may reveal cardiomegaly and pulmonary congestion (fluid
overload).
plain roentgenogram study of the abdomen, renal ultrasonography, and a radionuclide
scan
retrograde pyelography - needed to detect occult obstructions.
Renal biopsy to determine the precise cause of renal failure.

TREATMENT.

volume replacement -assessment of the state of hydration.

oliguric patients - distinguish whether oliguria is due to hypoperfusion (hypovolemia) or
impending acute tubular necrosis.
In patients with hypovolemia,
the urine is concentrated (urine osmolality > 500 mOsm/kg),
sodium content is usually less than 20 mEq/L,
fractional excretion of sodium (urine/plasma sodium concentration divided by the
urine/plasma creatinine concentration × 100 UNa/PNa = less than 1%.
UCr/PCr
In acute tubular necrosis,
urine is dilute (osmolality < 350 mOsm/kg),
sodium concentration usually exceeds 40 mEq/L (mmol/L),
fractional excretion of sodium usually exceeds 1%.

If there is hypovolemia intravascular volume is expanded by intravenous administration

of isotonic saline, 20 mL/kg, over 30 min. After this infusion, dehydrated patients
generally void within 2 hr. Failure to do so - re-evaluation of a patient.
Catheterization of the bladder and determination of the central venous pressure may be
helpful. Severe dehydration may require additional fluid IV. If clinical and laboratory
evaluations show that the patient is well hydrated, then diuretic therapy may be
considered.

Furosemide or mannitol or both may increase the rate of urine production.

furosemide administered as a single intravenous dose of 2 mg/kg at the rate of 4 mg/min
(to avoid ototoxicity); if no response occurs, a second dose of 10 mg/kg may be given. If
no urine comes further furosemide therapy is contraindicated.
A single intravenous dose of 0.5–1.0 g/kg of mannitol is given over 30 min in addition to
furosemide. No additional mannitol should be given
To increase renal cortical blood flow, dopamine (2 mg/kg/min) is administered (in the
absence of hypertension) with diuretic therapy.

Fluid restriction depends on the state of hydration. In oliguria or anuria and normal
intravascular volume, fluid administration should initially be limited to 400 mL/m2 /24 hr
(insensible losses) plus an amount of fluid equal to the urine output for that day.
In CCF - almost total fluid restriction; only replacement of insensible fluid losses Keep
IV canula and use infusion pump at the slowest possible rate.
Glucose-containing solutions (10–30%) without electrolytes are used as maintenance
fluids. The composition of the fluid may be modified in accordance with the state of
electrolyte balance.
Fluid intake, urine and stool output, and body weight should be monitored on a daily
basis.
hyperkalemia (serum level > 6 mEq/L) may lead to cardiac arrhythmia.
No potassium-containing fluid, foods, or medications until adequate renal function is re-
established. ECG - change seen is the
appearance of tall, peaked T waves.
ST-segment depression
prolongation of the P-R
widening of the QRS intervals
ventricular fibrillation
cardiac arrest.

Sodium polystyrene sulfonate resin (Kayexalate), 1 g/kg, given orally or by retention

enema. It exchanges sodium for potassium.
If the serum potassium rises above 7 mEq/L (mmol/L)--
Calcium gluconate 10% solution, 0.5 mL/kg IV, over 10 min. The heart rate must be
closely monitored during the infusion; a fall in rate of 20 beats/min requires stopping the
infusion until the pulse returns to the preinfusion rate.
Sodium bicarbonate 7.5% solution, 3 mEq/kg IV. Possible complications include volume
expansion, hypertension, and tetany.
Glucose 50% solution, 1 mL/kg, with regular insulin, 1 unit/5 g of glucose, given IV over
1 hr. Patients should be monitored closely for hypoglycemia.
Calcium gluconate does not lower the serum potassium but counteracts the potassium-
induced increase in myocardial irritability. Bicarbonate lowers serum potassium level; the
mechanism is not clearly defined. The effect of glucose and insulin is to shift potassium
from the extracellular to the intracellular compartment. b-Adrenergic receptor agonists
(Salbutamol)given by nebuliser also lowers potassium levels.
Persistent hyperkalemia, should be managed by dialysis.

Acidosis in renal failure is as a result of inadequate excretion of hydrogen ion and

ammonia.
Severe acidosis =arterial pH < 7.15, serum bicarbonate < 8 mEq/L may increase
myocardial irritability and requires treatment. Acidosis should be corrected only partially
by the intravenous route, giving enough bicarbonate to raise the arterial pH to 7.20
(which is a serum bicarbonate level of 12 mEq/L )
The remainder of the correction, should be accomplished only after normalization of the
serum calcium and phosphorus levels, by oral administration of sodium bicarbonate
tablets or sodium citrate solution.

correction of acidosis with intravenous bicarbonate may precipitate tetany

In patients with renal failure, an inability to excrete phosphorus leads to
hyperphosphatemia and hypocalcemia. Acidosis prevents the development of tetany by
increasing the ionized fraction of the total calcium. Rapid correction of acidosis reduces
the ionized calcium concentration, resulting in tetany.

Hypocalcemia is treated by lowering the serum phosphorus level. Unless tetany develops,
calcium is not given intravenously, in order to avoid reaching a calcium × phosphorus
product (mg/dL × mg/dL of 70) in the serum, the point at which calcium salts are
deposited in tissue.
To lower the serum phosphorus level, a phosphate-binding calcium carbonate antacid is
given by mouth, increasing fecal phosphate excretion
Hyponatremia is due to administration of hypotonic fluids to oliguric-anuric patients.
Correction by fluid restriction.
serum sodium levels below 120 mEq/L are at risk of developing cerebral edema and
central nervous system hemorrhage. In the absence of dehydration, water restriction is
essential. When the serum sodium falls below 120 mEq/L , it may be elevated to 125
mEq/L (mmol/L) by intravenous infusion of hypertonic (3%) sodium chloride

Risk of 3% saline- volume expansion, hypertension, and heart failure- may be treated by
dialysis.

Gastrointestinal bleeding - calcium carbonate antacids, -cimetidine - - dose of 5–10

mg/kg/12 hr.

Hypertension
primary disease process
expansion of the extracellular fluid volume
In patients with renal failure and hypertension, salt and water restriction is critical.

In children with severe acute symptomatic hypertension, diazoxide is a useful. - given by

rapid (< 10 sec) intravenous injection at a dose of 1–3 mg/kg (maximum dose of 150
mg). Blood pressure usually declines within 10–20 min
nifedipine may be given acutely (0.25–0.5 mg/kg PO).
Sodium nitroprusside - intravenous infusion is - for hypertensive crises.
salt and water restriction,
furosemide)
b-blockers -propranolol; 1–3 mg/kg/12 hr PO
vasodilators Apresoline , minoxidil are effective.

Seizures – causes -
primary disease process (systemic lupus erythematosus),
hyponatremia (water intoxication),
hypocalcemia (tetany),
hypertension,
cerebral hemorrhage,
uremic state.
Therapy should be directed toward the precipitating cause. Diazepam is the most
effective agent in controlling seizures. Its metabolic products are excreted in the urine
and may accumulate in patients with renal insufficiency.

Anemia

hemolysis (hemolytic-uremic syndrome, lupus)

bleeding,
The anemia of acute renal failure is mild (hemoglobin 9–10 g/dL),-does not require
transfusion.
Blood loss from active bleeding should be replaced appropriately--if hemoglobin below 7
g/dL, blood should be givenSlow (4–6 hr) transfusion with fresh (to minimize the amount
of potassium administered) packed red blood cells (10 mL/kg) diminishes the risk of
hypervolemia. Anemia should be corrected during dialysis.

The diet - restricted to fats and carbohydrates, Restriction of sodium, potassium, and
water is important. If renal failure persists beyond 3 days, then parenteral essential amino
acids may be needed.

Indications for dialysis in acute renal failure

acidosis,
electrolyte abnormalities (especially hyperkalemia)
central nervous system disturbances
hypertension
fluid overload
heart failure.

Hemofiltration is an extracorporeal therapy in which fluid, electrolytes, and small- and

medium-sized solutes are continuously removed from the blood by a process called
convection or ultrafiltration . In convection, water is moved by pressure through a
semipermeable membrane, bringing along other molecules (urea).
The filter, contains thousands of highly permeable hollow-fiber capillaries that produce a
filtrate that is similar to the glomerular filtrate (protein-free, solute concentration similar
to the plasma water).

Hemofiltration –
In continuous arteriovenous hemofiltration (CAVH), the blood is pumped through the
filter by the patient's heart; the driving force for filtration is the arterial blood pressure.
The advantage is that in the absence of a blood pump, filtration decreases or stops if the
blood pressure falls. Vascular access is by catheterization of the femoral artery and vein,
the brachial artery and jugular vein,.
In continuous venovenous hemofiltration (CVVH), blood is moved through the circuit by
a pump. The rate of filtrate formation is dependent on the pressure generated by the pump
speed and is independent of the blood pressure. Patient's blood pressure must be
continuously monitored. Only venous access is required, double-lumen catheters placed
into the subclavian or femoral veins may be used.

The life-threatening complications of uremia –

Hemorrhage
pericarditis,
central nervous system dysfunction
The risk of developing these complications correlates more closely with the level of BUN
than with that of creatinine.

PROGNOSIS.
The prognosis for recovery of renal function depends on the disorder that precipitated the
renal failure.
Recovery of function is good in prerenal causes, the hemolytic-uremic syndrome, acute
tubular necrosis, acute interstitial nephritis, or uric acid nephropathy.
Recovery of renal function is unusual when renal failure results from rapidly progressive
glomerulonephritis, bilateral renal vein thrombosis, or bilateral cortical necrosis.