Acute renal failure (ARF) is the generic term used to define an abrupt decrease in renal function sufficient to result in retention of nitrogenous waste (ex. BUN and creatinine) in the body. The hallmark of ARF is progressive azotemia caused by the accumulation of the nitrogenous end-products of metabolism. This accumulation is accompanied by a wide range of other disturbances depending on the severity and duration of the renal dysfunction. These include metabolic derangements such as metabolic acidosis and hyperkalemia, disturbances of body fluid balance, and effects on many other organ systems. ARF is commonly encountered in the practice of medicine, and 4-5% of hospital admissions to a general medical/surgical ward will go on to develop ARF. This disorder is less common in children than adults.

Abrupt renal decline and failure is a final common pathway for a number of disease processes and is associated with significant morbidity and mortality. Given the high frequency of this disease, the multiple causes, and the significant morbidity, a logical clinical approach to ARF is needed to help illuminate the cause and then to proceed to the proper therapy.

Etiology of Acute Renal Failure

The various etiologies of ARF can be grouped into three major categories:

* those that decrease renal blood flow (prerenal)

* those that produce a renal parenchymal insult (intrarenal)

* those that obstruct urine flow (postrenal or obstructive).

Identification of either a prerenal or postrenal cause of ARF makes the initiation of a specific therapy possible. If, however, these two categories can be ruled out, then an intrarenal cause can be implicated. The renal parenchymal causes of ARF are usually subdivided into those primarily affecting the glomeruli, the intrarenal vasculature, or the renal interstitium. The term acute tubular necrosis denotes another broad category of intrinsic renal failure that cannot be attributed to glomerular, vascular, or interstitial causes.

The complete list of the most common causes of acute renal failure is noted below in tables divided by major categories. The pathophysiology is also discussed.

Prerenal Causes of Acute Renal Failure:

Pathophysiology of Prerenal ARF: Results from a decrease in renal blood flow. The glomerular filtration rate (GFR) is reduced and the kidney retains water and salt, causing oliguria, production of a concentrated urine, and a progressive inability to excrete nitrogenous wastes.

Pathophysiology of Intrarenal Acute Renal Failure:

a) Glomerular Disease: Most of the glomerular disease producing ARF are felt to be immunologically mediated and result in disrupted glomerular filtration. Progression of the inflammatory process leads to destruction of glomerulus and a decrease in the GFR.

b) ATN: The exact cause of this is not clear.

c) Interstitial Disease: Interstitial nephritis is a complex collection of disease processes with a poorly understood pathophysiology. An inflammatory process is initiated in the renal interstitium in response to a wide variety of stimuli (toxic, metabolic, infectious, immune, infiltrative), although drugs are probably the most common causes.

Pathophysiology of Postrenal Acute Renal Failure: A simple mechanical or functional obstruction to the free flow of urine precludes its excretion, producing renal failure.

Treatment of Acute Renal Failure

The patient with acute renal failure may present extremely ill and sometimes moribund. There is almost no margin for error and the differential diagnosis can be extremely difficult. In spite of this, it is necessary to take a strict logical approach to the patient. First, resuscitate, next complete the differential diagnosis, then try etiologic treatment, and if that fails, prevent complications through the use of conservative and dialysis treatment.

Resuscitation: The two most common causes of death early in the resuscitative phase are hyperkalemia and pulmonary edema. Over hydration with resultant pulmonary edema is usually a result of iatrogenic as a result of futile attempts to restore urine output before the etiology of the renal failure has been established. At the same time that the patient is being hydrated and metabolic/electrolyte are being managed the etiology of the ARF needs to be established so that the needed interventions can begin.

Postrenal Failure: In those with postrenal failure, a passage for the drainage of urine must be created. The exact method that is used will depend entirely on the level of the obstruction and may be as simple as a urinary catheter ,or as complex as a percutaneous nephrostomy tube.

Prerenal Failure (Remember the etiologies):

Treatment for True Volume Depletion: Therapy for this type of ARF is aimed at restoration of the normal circulating blood volume. The major question that need to be addressed is the rate at which the fluid should be given. This usually depends on the clinical status of the patient. Initially fluid boluses may be needed, and if indicated blood transfusion may be required. The patient must be constantly reassessed to insure that the patient is not getting overhydrated. The adequacy of fluid repletion can be assessed from physical exam and by monitoring renal function and urine output.

Treatment for ARF due to Advanced Liver Disease: Dietary sodium restriction and periods of bed rest are the mainstays of nonmedical therapy in this disease entity. Medical therapies are as follows.

Diuretics therapy is often indicated and the preferred agent is spironolactone. Normally this is a fairly weak diuretic, however in cases of liver failure it is very effective. Spironolactone is the only diuretic that does not require secretion into the lumen of the kidney . Rather, it enters the collecting tubule cells from the blood side and competes for the aldosterone receptor. The rate of diuresis needs to be slow and steady.

Paracentesis may be helpful in those patients with tense ascities. Albumen may be given at the same time to help prevent the worsening of intravascular depletion. A peritoneovenous shunt, which drains into the internal jugular vein and translocates the ascitic fluid into the vascular space. The side effects are often severe.

Treatment of ARF Caused by Congestive Heart Failure: The use of diuretics may be of some help as this will increase the renal output. Another option is a trial of iatrogenic agents to help increase cardiac output and thus increase renal perfusion. ACE inhibitors may also be helpful although their benefit particularly in the Emergency Department setting is not proven.

Renal Causes of ARF: When prerenal and renal causes of ARF have been ruled out, the challenge becomes to identify the cause of the intrinsic renal failure, keeping in mind the multitude of known possible causes. Most commonly, the cause of the intrinsic renal failure will be from ATN.

Therapy in established ATN, other than correction of the underlying problem, is largely supportive. In particular, attention must be paid to maintenance of the fluid and electrolyte balance and to proper nutrition. Obviously, the former is the most important to the Emergency medicine physician. Despite management, some patients will require dialysis. Indications for dialysis include:

* marked fluid overload

* severe hyperkalemia

* presence of uremic signs or symptoms (pericarditis, N/V, confusion, bleeding with coagulopathy present)

* severe metabolic acidosis (controversial)

* BUN levels greater than 100

The use of diuretics may be able to convert oliguric ATN into nonoliguric ATN which has a better prognosis. Lasix can be used in high dose and a drip may be instituted if needed. Another agent which may be of benefit is mannitol. This drug may be helpful in those with worsening renal failure as well as preventing the development of ATN in those who have had an insult likely to cause this.

Finally, dopamine may be an effective agent along with furosimide in an effort to increase urine output.