Acute renal failure is an acute loss of kidney function that occurs over days to weeks and results in an inability to appropriately excrete nitrogenous wastes and creatinine. Electrolyte disturbances and loss of fluid homeostasis may occur. Accepted diagnostic criteria include an increase in the serum creatinine level of 0.5 mg per dL (44.2 µmol per L) or a 50 percent increase in the creatinine level above the baseline value, a 50 percent decrease in the baseline-calculated glomerular filtration rate (GFR), or the need for acute kidney replacement therapy. Oliguria is defined as a urine output of less than 400 mL in 24 hours, and anuria is defined as a urine output of less than 100 mL in 24 hours. Acute renal failure is present in 1 to 5 percent of patients at hospital admission. The condition affects 15 to 20 percent of patients in intensive care units (ICUs); reported mortality rates range from 50 to 70 percent in these patients. Infection and cardiorespiratory complications are the most common causes of death in patients with acute renal failure.
Causes of Acute Renal Failure
Traditionally, the causes of acute renal failure are classified as prerenal, intrarenal, or postrenal.
Prerenal Causes
Prerenal causes of acute renal failure are common, with intravascular volume depletion being the most common cause. Fever, vomiting, and diarrhoea can lead to decreased kidney perfusion. Dehydration from any cause, including diuretics, can precipitate acute renal failure.
Prerenal azotemia occurs in diseases that lead to a decrease in the effective arterial blood volume. These diseases include heart failure, liver failure, and nephrotic syndrome.
Nonsteroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitors are known to cause prerenal azotemia. NSAIDs affect the kidney by blocking cyclo-oxygenase, leading to an increase in thromboxane A2, which is a potent vasoconstrictor of the preglomerular arterioles. Because these afferent vessels supply blood to the kidney, vasoconstriction causes decreased glomerular perfusion.
ACE inhibitors block the production of angiotensin II, causing vasodilation of the postglomerular efferent arterioles. The vasodilation results in a decrease in the glomerular pressure, which may cause azotemia.
Large-vessel diseases, such as thrombosis, embolus, and dissection, also can reduce renal perfusion.
Intrarenal Causes
Intrarenal causes of acute renal failure are classified as tubular, glomerular, interstitial, and vascular.
Injury to the tubules most often is caused by ischemia or nephrotoxins. If prerenal azotemia and poor perfusion continue without treatment, tubular cells begin to die. This condition is termed “acute tubular necrosis.” Acute tubular necrosis is not a separate entity; rather, it is a marker of a more severe ischemic insult to the kidneys. Therefore, prerenal azotemia and tubular ischemia represent stages in the continuum of tubular injury.
Acute tubular necrosis has three phases: initiation, maintenance, and recovery. After the initial insult to the kidneys, the maintenance phase typically lasts one to two weeks. During the recovery phase, there may be marked diuresis and a slow return of kidney function. To date, no therapy has been shown to hasten recovery from acute tubular necrosis.
Efforts should be made to prevent the development of acute tubular necrosis in high-risk patients. Conditions that place patients at risk for this condition include untreated prerenal azotemia and the use of nephrotoxic drugs or exposure to other nephrotoxins
Postrenal causes
Postrenal causes of acute renal failure result in obstruction of the outflow tracts of the kidneys. Causes include prostatic hypertrophy, catheters, tumors, strictures, and crystals. The neurogenic bladder also can cause an obstruction.
Because postrenal causes are readily reversible, it is imperative to exclude them. Recovery of renal function is directly proportional to the duration of the obstruction. Renal ultrasonography can be used to assess patients for hydronephrosis because no contrast dye is used, renal function is not further compromised.