Acute Renal FailureAcute renal failure develops when renal function is diminished to the point where bodyfluid homeostasis can no longer be maintained.Oliguric renal failure --daily urine volume < 400 mL/m2 or 1ml/kg/hourNonoliguric renal failure --urine volume may approximate normal eg- aminoglycosidenephrotoxicity.Biochemical criteria for RF- blood urea nitrogen [BUN], Creatinine urine volumeETIOLOGY.Prerenal-- decreased perfusion of the kidneys results in decreased renal functionRenal --direct involvement of the kidneys,Postrenal is - primarily of obstructive disorders.PATHOGENESIS.Prerenal renal failure - decreased renal perfusion - decrease in the total circulating bloodvolume. No kidney damage. Diminished intravascular volume fall in cardiac output, decline in renal cortical blood flow and glomerular filtration rate (GFR). If underlyingcause of the hypoperfusion is reversed, then renal function may return to normal. Ifhypoperfusion persists beyond a critical point, then direct renal parenchymal damage maydevelop.Renal causes of acute renal failure -- - rapidly progressive forms of several types ofglomerulonephritis - causes - acute renal failure in older children. Activation of thecoagulation system within the kidneys, resulting in small vessel thrombosis, acuterenal failure. Acute dehydration and the hemolytic-uremic syndrome are the mostcommon causes of acute renal failure in toddlers.Acute tubular necrosis is acute renal failure in the absence of arterial or glomerularlesions. 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 tubularcells .Acute interstitial nephritis is due to hypersensitivity reaction to a therapeutic agent.Tumors infiltration of the kidneys or by obstruction of the tubules by uric acid crystalsDevelopmental abnormalities and hereditary nephritis Inability to conserve sodium andwater is common -If oral intake is compromised (vomiting) or extrarenal salt and waterloss develops (diarrhea), leads to intravascular volume contraction and renal failure.Postrenal causes of acute renal failure obstructions of the urinary tract. Ureteralobstruction must be bilateral to produce renal failure. Dilatation of the upper collectingsystem may take several days to develop in acute Ureteral obstruction.
CLINICAL MANIFESTATIONS.Clinical findings of the renal failure includepallor (anemia),diminished urine output,edema (salt and water overload),hypertension,vomiting,lethargy (uremic encephalopathy).Complications of acute renal failure CVS, GIT, CNSCVS --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 medicationsFlank masses -- renal vein thrombosis, tumors, cystic disease, or obstruction.Laboratory abnormalitiesanemia (with the rare exception of blood loss, the anemia is usually dilutional orhemolytic, as in lupus, renal vein thrombosis, and the hemolytic-uremic syndrome);leukopenia (lupus)thrombocytopenia (lupus, renal vein thrombosis, hemolytic-uremic syndrome);hyponatremia (dilutional)HyperkalemiaAcidosiselevated serum concentrations of BUNcreatinineuric acidphosphate (diminished renal function)hypocalcemia (hyperphosphatemia).The serum C3 level may be depressed (poststreptococcal, lupus, ormembranoproliferative glomerulonephritis)antibodies streptococcal (poststreptococcal glomerulonephritis), nuclear (lupus), neutrophil cytoplasmic antigens (ANCA; Wegeners granulomatosis, microscopicpolyarteritis), basement membrane (Goodpasture disease) antigens.Chest roentgenography may reveal cardiomegaly and pulmonary congestion (fluidoverload).
plain roentgenogram study of the abdomen, renal ultrasonography, and a radionuclidescanretrograde 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) orimpending 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 theurine/plasma creatinine concentration × 100 UNa/PNa = less than 1%. UCr/PCrIn 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 administrationof isotonic saline, 20 mL/kg, over 30 min. After this infusion, dehydrated patientsgenerally 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 behelpful. Severe dehydration may require additional fluid IV. If clinical and laboratoryevaluations show that the patient is well hydrated, then diuretic therapy may beconsidered.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. Ifno 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 tofurosemide. No additional mannitol should be givenTo increase renal cortical blood flow, dopamine (2 mg/kg/min) is administered (in theabsence of hypertension) with diuretic therapy.Fluid restriction depends on the state of hydration. In oliguria or anuria and normalintravascular 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 KeepIV canula and use infusion pump at the slowest possible rate.Glucose-containing solutions (10–30%) without electrolytes are used as maintenancefluids. The composition of the fluid may be modified in accordance with the state ofelectrolyte balance.Fluid intake, urine and stool output, and body weight should be monitored on a dailybasis.
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 retentionenema. 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 beclosely monitored during the infusion; a fall in rate of 20 beats/min requires stopping theinfusion until the pulse returns to the preinfusion rate.Sodium bicarbonate 7.5% solution, 3 mEq/kg IV. Possible complications include volumeexpansion, hypertension, and tetany.Glucose 50% solution, 1 mL/kg, with regular insulin, 1 unit/5 g of glucose, given IV over1 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; themechanism is not clearly defined. The effect of glucose and insulin is to shift potassiumfrom 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 andammonia.Severe acidosis =arterial pH < 7.15, serum bicarbonate < 8 mEq/L may increasemyocardial irritability and requires treatment. Acidosis should be corrected only partiallyby 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 theserum calcium and phosphorus levels, by oral administration of sodium bicarbonatetablets or sodium citrate solution.correction of acidosis with intravenous bicarbonate may precipitate tetanyIn patients with renal failure, an inability to excrete phosphorus leads tohyperphosphatemia and hypocalcemia. Acidosis prevents the development of tetany byincreasing the ionized fraction of the total calcium. Rapid correction of acidosis reducesthe 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 aredeposited in tissue.To lower the serum phosphorus level, a phosphate-binding calcium carbonate antacid isgiven by mouth, increasing fecal phosphate excretionHyponatremia 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 andcentral nervous system hemorrhage. In the absence of dehydration, water restriction isessential. When the serum sodium falls below 120 mEq/L , it may be elevated to 125mEq/L (mmol/L) by intravenous infusion of hypertonic (3%) sodium chlorideRisk of 3% saline- volume expansion, hypertension, and heart failure- may be treated bydialysis.Gastrointestinal bleeding - calcium carbonate antacids, -cimetidine - - dose of 5–10mg/kg/12 hr.Hypertension primary disease process expansion of the extracellular fluid volumeIn patients with renal failure and hypertension, salt and water restriction is critical.In children with severe acute symptomatic hypertension, diazoxide is a useful. - given byrapid (< 10 sec) intravenous injection at a dose of 1–3 mg/kg (maximum dose of 150mg). Blood pressure usually declines within 10–20 minnifedipine 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 POvasodilators 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 mosteffective agent in controlling seizures. Its metabolic products are excreted in the urineand 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 requiretransfusion.Blood loss from active bleeding should be replaced appropriately--if hemoglobin below 7g/dL, blood should be givenSlow (4–6 hr) transfusion with fresh (to minimize the amountof potassium administered) packed red blood cells (10 mL/kg) diminishes the risk ofhypervolemia. Anemia should be corrected during dialysis.The diet - restricted to fats and carbohydrates, Restriction of sodium, potassium, andwater is important. If renal failure persists beyond 3 days, then parenteral essential aminoacids 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- andmedium-sized solutes are continuously removed from the blood by a process calledconvection or ultrafiltration . In convection, water is moved by pressure through asemipermeable membrane, bringing along other molecules (urea).The filter, contains thousands of highly permeable hollow-fiber capillaries that produce afiltrate that is similar to the glomerular filtrate (protein-free, solute concentration similarto the plasma water).Hemofiltration –In continuous arteriovenous hemofiltration (CAVH), the blood is pumped through thefilter by the patients 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 theblood 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 bya pump. The rate of filtrate formation is dependent on the pressure generated by the pumpspeed and is independent of the blood pressure. Patients blood pressure must becontinuously monitored. Only venous access is required, double-lumen catheters placedinto the subclavian or femoral veins may be used.The life-threatening complications of uremia – Hemorrhage pericarditis, central nervous system dysfunctionThe risk of developing these complications correlates more closely with the level of BUNthan with that of creatinine.PROGNOSIS.
The prognosis for recovery of renal function depends on the disorder that precipitated therenal failure.Recovery of function is good in prerenal causes, the hemolytic-uremic syndrome, acutetubular necrosis, acute interstitial nephritis, or uric acid nephropathy.Recovery of renal function is unusual when renal failure results from rapidly progressiveglomerulonephritis, bilateral renal vein thrombosis, or bilateral cortical necrosis.