Acute renal failure, the sudden interruption of renal function, can be caused by obstruction, poor circulation, or underlying kidney disease. It may be prerenal, intrarenal, or postrenal in origin; it usually passes through three distinct phases: oliguric, diuretic, and recovery.
Causes
Prerenal failure
· Arrhythmias, cardiac tamponade, cardiogenic shock, heart failure, myocardial infarction
· Burns, trauma, sepsis, tumor
· Dehydration, hypovolemic shock
· Diuretic overuse, antihypertensive drugs
· Hemorrhage, arterial embolism, arterial or venous thrombosis, vasculitis
· Disseminated intravascular coagulation
· Eclampsia, malignant hypertension
Intrarenal failure
· Poorly treated prerenal failure
· Nephrotoxins
· Obstetric complications
· Crush injuries
· Myopathy
· Transfusion reaction
· Acute glomerulonephritis, acute interstitial nephritis, acute pyelonephritis, bilateral renal vein thrombosis, malignant nephrosclerosis, papillary necrosis
· Polyarteritis nodosa
· Renal myeloma
· Sickle cell disease
· Systemic lupus erythematosus
· Vasculitis
Postrenal failure
· Bladder, ureteral, or urethral obstruction
Pathophysiology
Prerenal failure is caused by a condition that diminishes blood flow to the kidneys, leading to hypoperfusion. Hypoperfusion leads to hypoxemia, which can rapidly damage the kidney. The tubules are most susceptible to hypoxemia's effect. The impaired blood flow results in decreased glomerular filtration rate (GFR) and increased tubular reabsorption of sodium and water. Electrolye imbalances and metabolic acidosis result.
Intrarenal failure, also called intrinsic or parenchymal renal failure, results from damage to the filtering structures of the kidneys. Nephrotoxicity or inflammation damage the delicate layer under the epithelium (basement membrane) and it becomes irreparibly damaged, leading to chronic renal failure. Use of nephrotoxins also causes acute renal failure because they accumulate in the renal cortex.
Postrenal failure is a consequence of bilateral obstruction of urine outflow. The cause may be in the bladder, ureters, or urethra.
Signs and symptoms
· Oliguria or anuria
· Tachycardia and hypotension
· Dry mucous membranes and flat neck veins
· Lethargy
· Cool, clammy skin
Progressive disease
· Edema
· Confusion
· GI symptoms
· Crackles
· Infection
· Seizures and coma
· Hematuria, petechiae, ecchymosis
Diagnostic test results
· Blood studies show elevated blood urea nitrogen, serum creatinine, and potassium levels; decreased bicarbonate level, hematocrit, and hemoglobin levels; and low blood pH.
· Urine studies show casts, cellular debris, and decreased specific gravity; in glomerular diseases, proteinuria and urine osmolality close to serum osmolality; urine sodium level less than 20 mEq/L if oliguria results from decreased perfusion and more than 40 mEq/L if the cause is intrarenal.
· Creatinine clearance test measures GFR and reflects the number of remaining functioning nephrons.
· Electrocardiogram (ECG) shows tall, peaked T waves; widening QRS complex; and disappearing P waves if hyperkalemia is present.
· Ultrasonography, plain films of the abdomen, kidney-ureter-bladder radiography, excretory urography, renal scan, retrograde pyelography, computed tomography scans, and nephrotomography are used to investigate the cause of renal failure.
Treatment
· High-calorie diet low in protein, sodium, and potassium
· Electrolyte imbalance: I.V. fluids and electrolytes; hemodialysis or peritoneal dialysis if needed; continuous renal replacement therapies
· Edema: fluid restriction
· Oliguria: diuretic therapy
· With mild hyperkalemic symptoms (malaise, anorexia, muscle weakness): sodium polystyrene sulfonate by mouth or enema
· With severe hyperkalemic symptoms (numbness and tingling and ECG changes): hypertonic glucose, insulin, and sodium bicarbonate I.V.
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MECHANISM OF ACUTE RENAL FAILURE
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