Acute renal failure (ARF) is a sudden impairment of a patients renal capability to excrete nitrogenous wastes, and if impairment is severe enough or not corrected in a timely manner, excessive accumulation of these waste products may result in uremia. In ARF, the glomerular filtration rate (GFR) decreases rapidly over hours or just a few days. Therefore, the trend of a patients BUN and creatinine is extremely important. A sudden rise from normal or from a known baseline impairment in patients with chronic renal insufficiency is characteristic of ARF. Other clues to the distinction between acute and chronic renal failure are a normal hemoglobin/hematocrit (patients with chronic renal failure characteristically have a normocytic anemia) and normal sized kidneys (greater than nine centimeters) on renal ultrasound, both of which support the diagnosis of ARF. The four conditions in which chronic renal failure is associated with normal or large sized kidneys on ultrasound examination are diabetic nephropathy, amyloidosis-associated renal disease, polycystic kidney disease, and when there is concomitant hydronephrosis. There are three broad categories of ARF, prerenal, renal (or parenchymal), and postrenal.
Prerenal ARF is caused by renal hypoperfusion. The renal parenchyma is functional but insufficient blood flow to the kidneys disrupts maintenance of a normal GFR. Prerenal azotemia may result from hypovolemia, an impaired cardiac output, or bilateral renal artery stenosis. When patients present with ARF, it is important to first determine if it is prerenal and if so to further determine the underlying etiology. This is extremely important as rapid volume correction in hypovolemic patients may return renal function to normal, but a delay in therapy may cause ischemic parenchymal damage resulting in acute tubular necrosis and prolong the course of renal failure. In hypovolemic prerenal azotemia, the elevations in BUN and creatinine normalize quickly following fluid bolus with normal saline. This correction is considered diagnostic. Prerenal ARF secondary to a decrease in cardiac output with resultant renal hypoperfusion (congestive heart failure, cardiac tamponade, myocardial infarction, etc.) may correct with improvement of cardiac performance. Positive orthostatic vital signs (indicative of hypovolemia ) and oliguria not associated with obstruction are strong evidence from the physical exam which help support the diagnosis of prerenal ARF. A random urine sample should also be sent for determination of the sodium and creatinine content and also for osmolality. A urine sodium level less than 20 and an osmolality greater than 500 are characteristic of ARF secondary to renal hypoperfusion as is a fractional excretion of sodium (FENa) less than one.
Renal or parenchymal ARF results when hypovolemic prerenal azotemia is not corrected rapidly resulting in ischemic acute tubular necrosis (ATN), when nephrotoxins damage the kidney tubules resulting in nephrotoxic ATN (radiocontrast dye, aminoglycosides, rhabdomyolysis ), when patients suffer an allergic reaction of the kidney parenchyma to certain medications known as acute interstitial nephritis (AIN) or secondary to disease of the glomeruli, vasculature, or interstitium. Renal ARF may be categorized as oliguric or nonoliguric. Oliguria indicates a decreased urine output less than 20 ml/hour or less than 500 ml/day. This distinction is important because patients with nonoliguric acute renal failure have a better prognosis. Furthermore, if patients develop oliguric ARF, conversion to the nonoliguric form with diuretics does not improve prognosis. There are three phases of ATN: the renal failure phase, the diuretic phase, and the recovery phase. In patients with parenchymal ARF it is imperative to search for a history of recent radiocontrast dye or aminoglycoside administration or signs of recent or underlying infection as this may reveal the etiology. A serum creatinine phosphokinase (CPK) should be obtained to search for rhabdomyolysis induced ATN, and samples of both blood and urine should be monitored for signs of eosinophilia. This is accomplished in the urine sample by a Wrights stain or Hansels stain. Evidence of eosinophilia in a patient with fever and a rash is strong evidence to support the diagnosis of acute interstitial nephritis (AIN), which may respond well to treatment with steroids. Acute renal injury may be from a primary glomerulonephritis or secondary to an underlying disease. Multiple disease states are associated with acute renal injury such as systemic lupus erythematosus, Wegener's granulomatosis, microscopic polyangiitis, Goodpasture's syndrome, IgA nephropathy, streptococcal infections, etc.
The third type of ARF is postrenal or obstruction. Obstruction may occur below the bladder (urethral obstruction) or above the bladder in the ureters or renal pelvis. A common cause in male patients is prostatic obstruction secondary to benign prostatic hypertrophy ( BPH ) or prostate cancer. High obstruction must be bilateral to cause ARF as a nonobstructed kidney, if it is without underlying pathology, will be capable of increasing its GFR and filtering all of the serum waste products (compensatory hyperfiltration) in cases of unilateral ureteral obstruction. Initial evaluation in ARF patients includes placing a catheter into the bladder. If this yields a large volume of urine, renal function may be monitored and if it normalizes, then urethral obstruction is the diagnosis and its etiology should be determined. Once urethral obstruction is overcome, the bladder should be drained slowly over hours to avoid hypothermia. Intravenous fluids should be used to replace the volume of urine output as post-obstructive diuresis may be severe and result in dehydration. If placement of the catheter yields low urine volume then an obstruction at a higher level must be sought. A renal ultrasound searching for bilateral hydronephrosis or other pathology should be obtained.