Chapter 50. Acute Renal Failure

Renal dysfunction and acute renal failure present with a wide variety of manifestations, depending on the underlying etiology. Although the initial symptoms may be those of the primary cause, ultimately patients will develop deterioration of renal function. Renal failure can be caused by hypovolemia from any cause, cardiac disease, vascular or thrombotic disorders, glomerular diseases, diseases affecting the renal tubules, nephrotoxic drugs, and a variety of anatomic problems of the genitourinary tract.

Deterioration in renal function leads to excessive accumulation of nitrogenous waste products in the serum. Patients usually have signs and symptoms of their underlying causative disorder but eventually develop stigmata of renal failure. Volume overload, hypertension, pulmonary edema, mental status changes or neurologic symptoms, nausea and vomiting, bone and joint problems, anemia, and increased susceptibility to infection (a leading cause of death) can occur as patients develop more chronic uremia.

History and physical examination usually provide clues to etiology. Signs and symptoms of the underlying causative disorder should be vigorously sought. Physical examination should assess vital signs, volume status, establish urinary tract patency and output, and search for signs of chemical intoxication, drug usage, muscle damage, infections, or associated systemic diseases. Diagnostic studies include urinalysis, blood urea nitrogen and creatinine levels, serum electrolytes, urinary sodium and creatinine, and urinary osmolality. Analysis of these tests allows most patients to be categorized as prerenal, renal, or postrenal. Fractional excretion of sodium can be calculated to help in this categorization (Table 50-1). Normal urinary sediment may be seen in prerenal and postrenal failure, hemolytic-uremic syndrome, and thrombotic thrombocytopenic purpura. The presence of albumin may indicate glomerulonephritis or malignant hypertension. Granular casts are seen in acute tubular necrosis. Albumin and red blood cell casts are found in glomerulonephritis, malignant hypertension, and autoimmune disease. White blood cell casts are seen in interstitial nephritis and pyelonephritis. Crystals can be present with renal calculi and certain drugs (sulfas, ethylene glycol, and radiocontrast agents). Renal ultrasound is the radiologic procedure of choice in most patients with renal failure when upper tract obstruction and hydronephrosis is suspected. Color flow Doppler can assess renal perfusion and diagnosis large vessel causes of renal failure. Bedside sonography can quickly diagnose some treatable causes and give guidance for fluid resuscitation; inspiratory collapse of the intrahepatic IVC can give a good measure of volume status and fluid responsiveness (see Fig. 50-1).

Prerenal failure is produced by conditions that decrease renal perfusion and is the most common cause of community-acquired acute renal failure (70% of cases). It also is a common precursor to ischemic and nephrotoxic causes of intrinsic renal failure. Common causes of prerenal failure include hypovolemic states (vomiting/diarrhea, diuretics and other antihypertensives, reduced intake), fluid sequestration (cirrhosis, pancreatitis, burns, septic shock, others) blood loss, or decreased cardiac output from cardiac dysfunction. Intrinsic renal failure has vascular and ischemic etiologies; glomerular and tubulointerstitial diseases are also causative. Ischemic renal failure, traditionally known as acute tubular necrosis (ATN), is now called acute kidney injury. ATN, due to severe and prolonged prerenal etiologies, causes most cases of intrinsic renal failure; ATN is also the most common cause of hospital-acquired renal failure. Nephrotoxins (both physician prescribed and environmental) are the second most common cause of ATN. Postrenal azotemia occurs primarily in elderly men with high-grade prostatic obstruction. Lesions of the external genitalia (ie, strictures) are also common causes. Significant permanent loss of renal function occurs over 10 to 14 days with complete obstruction, and worsens with associated UTI. See the parent chapter in Tintinalli's 7th edition for a more complete list.

ED goals in the initial care of patients with acute renal failure focus on treating the underlying cause and correcting fluid and electrolyte derangements. Efforts should be made to prevent further renal damage and provide supportive care until renal function has recovered (see Chapter 4 for treatment of electrolyte and acid-base disorders).

Prerenal Failure

1. Effective intravascular volume should be restored with isotonic fluids (normal saline or lactated Ringer solution) at a rapid rate in appropriate patients; volume resuscitation is the first priority.

2. If cardiac failure is causing prerenal azotemia, cardiac output should be optimized to improve renal perfusion, and reduction in intravascular volume (ie, with diuretics) may be appropriate.

Renal Failure (Intrinsic)

Adequate circulating volume must be restored first; hypovolemia potentiates and exacerbates all forms of renal failure. Ischemia or nephrotoxic agents are the most common causes of intrinsic renal failure. History, physical examination, and baseline laboratory tests should provide clues to the diagnosis. Nephrotoxic agents (drugs and intravenous contrast) should be avoided.

1. Low-dose dopamine (1 to 5 micrograms/kilogram/min) may improve renal blood flow and urine output, but it does not lower mortality rates or improve recovery.

2. Renally excreted drugs (digoxin, magnesium, sedatives, and narcotics) should be used with caution because therapeutic doses may accumulate to excess and cause serious side effects. Fluid restriction may be required. Interventions useful in the prevention of radiocontrast nephropathy include acetylcysteine, fenoldopam, and crystalloid infusions.

Postrenal Failure

Appropriate urinary drainage should be established; the exact procedure depends on the level of obstruction.

1. A Foley catheter should be placed to relieve obstruction caused by prostatic hypertrophy. There is no support for the practice of intermittent catheter clamping to prevent hypotension and hematuria; urine should be completely and rapidly drained.

2. Percutaneous nephrostomy may be required for ureteral occlusion until definitive surgery to correct the obstruction can take place once the patient is stabilized.

3. For the acutely anuric patient, obstruction is the major consideration. If no urine is obtained on initial bladder catheterization, emergency urologic consultation should be considered.

4. With chronic urinary retention, postobstructive diuresis may occur due to osmotic diuresis or tubular dysfunction. Patients may become suddenly hypovolemic and hypotensive. Urine output must be closely monitored, with appropriate fluid replacement.

Dialysis

If treatment of the underlying cause fails to improve renal function, hemodialysis or peritoneal dialysis should be considered.

1. The nephrology consultant usually makes decisions about dialysis. Dialysis often is initiated when the blood urea nitrogen is greater than 100 milligrams/dL or serum creatinine is greater than 10 milligrams/dL.

2. Patients with complications of acute renal failure such as cardiac instability (due to metabolic acidosis and hyperkalemia), intractable volume overload, hyperkalemia, and uremia (ie, encephalopathy, pericarditis, and bleeding diathesis) not easily corrected by other measures should be considered for emergency dialysis. However, morality in renal failure has changed little since the advent of dialysis.

Disposition

Patients with new onset renal failure usually require hospital admission, often to an intensive care unit. Transferring patients to another institution should be considered if nephrology consultation and dialysis facilities are not available.