Each type of acute renal failure has a separate cause. Prerenal failure results from conditions that diminish blood flow to the kidneys. Between 40% and 80% of all cases of acute renal failure are caused by prerenal azotemia. Intrarenal failure (also called intrinsic or parenchymal renal failure) results from damage to the kidneys themselves, usually from acute tubular necrosis. Postrenal failure results from bilateral obstruction of urine outflow. (See Causes of acute renal failure, page 788.)

Ischemic acute tubular necrosis can lead to renal shutdown. Electrolyte imbalance, metabolic acidosis, and other severe effects follow as the patient becomes increasingly uremic, and renal dysfunction disrupts other body systems. If left untreated, the patient will die. Even with treatment, the elderly patient is particularly susceptible to volume overload, precipitating acute pulmonary edema, hypertensive crisis, hyperkalemia, and infection.

The patient’s history may include a disorder that can cause renal failure, and he may have a recent history of fever, chills, central nervous system problems such as headache, and GI problems such as anorexia, nausea, vomiting, diarrhea, and constipation.

The patient may appear irritable, drowsy, and confused or demonstrate other alterations in his level of consciousness. In advanced stages, seizures and coma may occur. Depending on the stage of renal failure, his urine output may be oliguric (less than 400 ml/24 hours) or anuric (less than 100 ml/24 hours).

Inspection may uncover evidence of bleeding abnormalities, such as petechiae and ecchymoses. Hematemesis may occur. The skin may be dry and pruritic and, rarely, you may note urea frost. Mucous membranes may be dry, and the patient’s breath may have a uremic odor. If the patient has hyperkalemia, muscle weakness may occur.

Auscultation may detect tachycardia and, possibly, an irregular rhythm. Bibasilar crackles may be heard if the patient has heart failure.

Palpation and percussion may reveal abdominal pain, if pancreatitis or peritonitis occurs, and peripheral edema, if the patient has heart failure.

Blood test results indicating acute intrarenal failure include elevated blood urea nitrogen, serum creatinine, and potassium levels as well as low blood pH, bicarbonate, hematocrit, and hemoglobin levels.

Urine specimens show casts, cellular debris, decreased specific gravity and, in glomerular diseases, proteinuria and urine osmolality close to serum osmolality. The urine sodium level is under 20 mEq/L if oliguria results from decreased perfusion and above 40 mEq/L if it results from an intrarenal problem. A creatinine clearance test measures the glomerular filtration rate and allows for an estimate of the number of remaining functioning nephrons.

Other studies that help determine the cause of renal failure include kidney ultrasonography, plain films of the abdomen, kidney-ureter-bladder radiography, excretory urography, renal scan, retrograde pyelography, computed tomography scans, and nephrotomography.

An electrocardiogram (ECG) shows tall, peaked T waves, a widening QRS complex, and disappearing P waves if hyperkalemia is present.

Supportive measures include a diet high in calories and low in protein, sodium, and potassium, with supplemental vitamins and restricted fluids. Meticulous electrolyte monitoring is essential to detect hyperkalemia. If hyperkalemia occurs, acute therapy may include hypertonic glucose-and-insulin infusions and sodium bicarbonate—all administered I.V. Another option to manage hyperkalemia
is the administration of sodium polystyrene sulfonate by mouth or enema to remove potassium from the body.