Acute Renal Failure

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 à fall in cardiac output, à 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, à 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 à 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 àobstructions 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.