Renal failure, acute

Obstruction, reduced circulation, and renal parenchymatous disease can all cause sudden interruption of kidney function. Acute renal failure is usually reversible with medical treatment; otherwise, it may progress to end-stage renal disease, uremic syndrome, and death.

Causes

Acute renal failure can be classified as prerenal, intrinsic (or parenchymatous), or postrenal.

Prerenal failure

Diminished blood flow to the kidneys causes prerenal failure. Such decreased flow may result from hypovolemia, shock, embolism, blood loss, sepsis, pooling of fluid in ascites or burns, or a cardiovascular disorder, such as heart failure, arrhythmias, and tamponade. Other causes include disorders of the blood, such as idiopathic thrombocytopenic purpura, transfusion reactions, and other hemolytic disorders; malignant hypertension; and disorders resulting from childbirth-like bleeding (associated with placental abruption or placenta previa) that can damage the kidneys. Autoimmune disorders, such as scleroderma, can also cause acute renal failure.

Intrinsic renal failure

Parenchymatous, or intrinsic, renal failure results from damage to the kidneys themselves, usually resulting from acute tubular necrosis. Such damage may also result from acute poststreptococcal glomerulonephritis, systemic lupus erythematosus, polyarteritis nodosa, vasculitis, sickle cell disease, bilateral renal vein thrombosis, nephrotoxins, ischemia, renal myeloma, and acute pyelonephritis.

Postrenal failure

Bilateral obstruction of urine outflow results in postrenal failure. Possible causes include renal calculi, clots, papillae from papillary necrosis, tumors, benign prostatic hyperplasia, strictures, and urethral edema from catheterization.

Signs and symptoms

Acute renal failure is a critical illness. Its early signs are oliguria, azotemia and, rarely, anuria. Electrolyte imbalances, metabolic acidosis, and other severe effects follow as the patient becomes increasingly uremic and renal dysfunction disrupts other body systems:

❑ GI — anorexia, nausea, vomiting, diarrhea or constipation, stomatitis, bleeding, hematemesis, dry mucous membranes, uremic breath

❑ central nervous system (CNS) — headache, drowsiness, irritability, confusion, peripheral neuropathy, seizures, coma

❑ cutaneous — dryness, pruritus, pallor, purpura; rarely, uremic frost

❑ cardiovascular — early in the disease, hypotension; later, hypertension, arrhythmias, fluid overload, heart failure, systemic edema, anemia, altered clotting mechanisms

❑ respiratory — Kussmaul’s respirations, pulmonary edema.

Fever and chills indicate infection, a common complication.

Diagnosis

The patient’s history may include a disorder that can cause renal failure. Blood test results indicating intrinsic acute renal failure include elevated urea nitrogen, creatinine, and potassium levels; low bicarbonate and hemoglobin (Hb) levels; and low pH and hematocrit (HCT).

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 less than 20 mEq/L if oliguria results from decreased perfusion and more than 40 mEq/L if it results from an intrinsic problem.

Other studies include renal ultrasonography, kidney-ureter-bladder radiography, cautious use of excretory urography, renal scan, retrograde pyelography, and nephrotomography.

Treatment

The goals of treatment include identifying and treating reversible causes, such as nephrotoxic drug therapy, obstructive uropathy, and volume depletion. 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 dialysis, hypertonic glucose and insulin infusions, and calcium — all administered I.V. — and oral or rectal administration of potassium exchange resin to remove potassium from the body.

If measures fail to control uremic symptoms, hemodialysis or peritoneal dialysis may be necessary.

Special considerations

❑ Measure and record intake and output, including all body fluids, such as wound drainage, nasogastric output, and diarrhea. Weigh the patient daily.

❑ Assess HCT and Hb levels, and replace blood components as needed. Don’tuse whole blood if the patient is prone to heart failure and can’t tolerate extra fluid volume.

❑ Monitor vital signs. Watch closely for signs and symptoms of pericarditis (such as pleuritic chest pain, tachycardia, and pericardial friction rub), inadequate renal perfusion (such as hypo-tension), and acidosis.

❑ Maintain proper electrolyte balance. Strictly monitor potassium levels.

CLINICAL TIP: Monitor the patient for hyperkalemia. Signs and symptoms include malaise, anorexia, paresthesia, muscle weakness, and electrocardiogram changes (such as tall, peaked T waves; widening QRS complex; and disappearing P waves). Don’t give any drug that contains potassium.

❑ Assess the patient frequently, especially during emergency treatment to lower potassium levels. If the patient receives hypertonic glucose and insulin infusions, monitor potassium levels. If you give sodium polystyrene sulfonate rectally, make sure the patient doesn’t retain it and become constipated, which could lead to bowel perforation.

❑ Maintain nutritional status. Provide a high-calorie, low-protein, low-sodium, low-potassium diet, with vitamin supplements. Give the patient with anorexia small, frequent meals.

❑ Prevent complications of immobility by encouraging frequent coughing and deep breathing and by performing passive range-of-motion exercises. Help the patient walk as soon as possible. Add lubricating lotion to the patient’s bathwater to combat skin dryness.

❑ Provide frequent mouth care to prevent dry mucous membranes. If stomatitis occurs, the patient may need an antibiotic solution. Have the patient swish the solution around in his mouth before swallowing.

❑ Use appropriate safety measures, such as side rails and restraints; the patient with CNS involvement may be dizzy or confused.

❑ Provide emotional support to the patient and his family. Reassure them by clearly explaining all procedures.

❑ During peritoneal dialysis, position the patient carefully. Elevate the head of the bed to reduce pressure on the diaphragm and aid respiration. Be alert for signs of infection (such as cloudy drainage and elevated temperature) and bleeding.

❑ If pain occurs, reduce the amount of dialysate. If the patient has diabetes, periodically monitor his blood glucose level, and administer insulin as needed. Watch for complications, such as peritonitis, atelectasis, hypokalemia, pneumonia, and shock.

❑ If the patient requires hemodialysis, check the blood access site (an arterio-venous fistula or a subclavian or femoral catheter) every 2 hours for patency and signs of clotting. Don’t use the arm with the shunt or fistula for taking blood pressures or drawing blood. Weigh the patient before beginning dialysis.

❑ During dialysis, monitor vital signs, clotting times, blood flow, the function of the vascular access site, and arterial and venous pressures. Watch for complications, such as septicemia, embolism, hepatitis, and rapid fluid and electrolyte loss.

❑ After dialysis, monitor vital signs and the vascular access site, weigh the patient, and watch for signs of fluid and electrolyte imbalances.

Book Source Details

• Book Title: Handbook of Diseases
• Author(s): Springhouse
• Year of Publication: 2003
• Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.

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Copyright Details: Handbook of Diseases, Copyright © 2008 Williams & Wilkins.

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• Back to symptom: Kidney damage: Introduction (review 195 causes)
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More About This Book: Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5

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