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Definition
• Acute renal failure is defined as sudden, rapid, potentially reversible deterioration of renal function.
• Hepatorenal syndrome
• Acute tubular necrosis – which accounts for about 75% of all cases of acute renal failure
• Acute glomerulonephritis
• Acute pyelonephritis
Postrenal obstruction
III. Pathophysiology
• The exact pathogenesis of acute renal failure is not always known, but it is associated with a severe
reduction in the glomerular filtration rate. This may be caused by decreased renal blood flow that leads
to increased renal-vascular resistance, increased hydrostatic pressure in Bowman’s capsule, or a
disruption of tubular epithelium.
• The onset phase – extends from the time of the precipitating event to the beginning of the oliguric-
anuric phase.
• The oliguric-anuric phase – is marked by urine output of less than 400 ml/day, volume overload,
elevated blood urea nitrogen (BUN) and creatinine levels, electrolyte abnormalities, metabolic acidosis,
and uremia.
• The diuretic phase – extends from the time that output becomes more than 400ml/day to the time the
BUN stops rising and stabilizes in normal range. During this phase, electrolyte and acid-base problems
begin to normalize.
• The convalescent phase – extends from the time the BUN stabilizes until the client returns to normal
activity. The client may take up to 2 years to regain 70%to 80% of normal function.
Systemic effects of acute renal failure are widespread and may include:
• Acidosis
• Platelet dysfunction
• Pericarditis
• Uremic encephalopathy
• Hypertension or hypotension
• Tachypnea
Urinalysis
Urine osmolality
Blood analysis
V. Medical Management
• Treatment objectives are to restore normal chemical balance and prevent complications until renal
tissues are repaired and renal function is restored. Possible causes of damage are identified and treated.
• Fluid balance is managed based on daily weight, serial measurements of central venous pressure,
serum and urine concentrations, fluid losses, blood pressure, and clinical status. Fluid excesses are
treated with mannitol, furosemide to initiate dieresis and prevent or minimize subsequent renal failure.
• Blood flow is restored to the kidneys with the use of intravenous fluids, albumin or blood product
transfusions.
• Intravenous glucose and insulin or calcium glutamate as an emergency and temporary measure to
treat hyperkalemia.
• Parenteral erythropoietin (Epogen) to treat reduced erythropoietin production and prevent anemia
• Dietary protein is limited to about 1g/kg during oliguric phase to minimize protein breakdown and to
prevent accumulation of toxic end products.
• Foods and fluids containing potassium and phosphorus are restricted; potassium intake is limited to 40
to 60 mEq/d. Sodium intake is restricted to 2 g/d.
• Blood chemistries are evaluated to determine amount of replacement sodium, potassium, and water
during oliguric phase.
• After the diuretic phase, high-protein, high-calorie diet is given with gradual resumption of activities.
Prevent GI bleeding by administering histamine receptor antagonists and proton pump inhibitors.
Promote comfort and encourage bed rest to reduce exertion and metabolic rate. As prescribed,
administer short-acting barbiturates to control pain, and assess for central nervous system
complications such as drowsiness, confusion, delirium, coma, and convulsions.
Provide a high-calorie and low-protein diet, with hyperalimentation if the client cannot eat.
If indicated, prepare the client for dialysis to correct hyperkalemia, fluid overload, acidosis, or
severe uremia.
Administer prescribed medication, which may include alkalinizing agents, antibiotics,
phosphate-binding agents, ion exchange resins, calcium supplements, histamine receptor
antagonists, and proton-pump inhibitors.
Promote measures to maintain fluid balance. Assess fluid balance, and restrict intake to 24-hour
urine output plus 500 ml/day.
Promote measures to ensure normal sodium and phosphate levels. Instruct the client to restrict
sodium intake, drink plenty of fluids, and follow a low-phosphate diet.
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