Acute renal failure occurs when renal function suddenly declines to very low levels, so that little or no urine is formed, and the substances, including even water, that the kidney normally eliminates are retained in the body.

There are two main mechanisms that can produce acute renal failure :

     1.  When the cardiac output--the amount of blood pumped into the general circulation by the heart--is lowered by hemorrhage or by medical or surgical shock, the renal circulation is depressed to an even greater extent. This leads directly to inefficient excretion, but, more importantly still, the kidney tissue cannot withstand prolonged impairment of its blood supply and undergoes either patchy or massive necrosis (tissue death). Given time, the kidney tissue may regenerate, and it is on this hope that the treatment of acute renal failure is based.

                     The form of acute renal failure that is due to a poor supply of blood (ischemia) has many causes, the most common and most important being multiple injuries, septicemia (infections invading the bloodstream), abortion with abnormal or excessive bleeding from the female genital tract, internal or external hemorrhage, loss of fluid from the body as in severe diarrhea or burns, transfusion reactions, and severe heart attacks; a special case is the transplanted kidney, which commonly goes through a phase of acute renal failure that is independent of possible rejection.
 

   2.  The second common mechanism of acute renal failure is toxic. Many poisons are excreted by the kidney, and in the process, like other urinary constituents, they become concentrated and thus reach levels in the tubular fluid that damage the lining cells of the tubules. Though the tubular cells die and are shed in the urine, regeneration can take place and the patient survive, if he can be maintained during the period of depressed renal function and is not killed by other effects of the poison. Poisons that can affect the kidney in this way are numerous, but the main groups are heavy metals (mercury, arsenic, uranium); organic solvents (carbon tetrachloride, propylene glycol, methanol); other organic substances (aniline, phenindione, insecticides); and antibacterial agents (sulfonamides, aminoglycosides, amphotericin), and some fungi (e.g., Amanita phalloides). In addition to the ischemic and toxic causes of acute renal failure, mention must be made of fulminating varieties of acute renal illnesses that are generally mild (e.g., acute glomerulonephritis--see below) and of the acute form of immunologic rejection that can destroy a kidney irrevocably within minutes of transplantation. Acute obstruction to the flow of urine from the kidneys obviously also can imperil renal function.
 

   The course of acute renal failure can usefully be divided into three phases: an onset phase, a phase of established acute renal failure, and a recovery phase. In general, but not invariably, the second of these phases is characterized by a low output of urine (oliguria) and the third by an increasing urine output (polyuria). The onset phase is dominated by general illness, in which the episode of acute renal failure arises; at this stage there may be evidence of threatened renal damage such as blood in the urine or pain in the loins. At this early stage, renal damage may be reversible by prompt treatment of circulatory failure (e.g., by the transfusion of adequate amounts of plasma, whole blood, or electrolyte replacement fluids) and by maintaining adequate blood oxygen levels. Infection or any underlying causative disorder also must be treated quickly.
In the second phase, small amounts of urine, often containing red blood cells, or hemoglobin, are passed; complete absence of urine is not common and suggests that an obstruction is preventing urine from being passed. In quantitative terms, a urine volume of less than 500 millilitres per day constitutes significant oliguria; this is the least amount in which the excretory demand imposed by an ordinary diet can be met. In the actual situation of acute renal failure, the excretory demands may in fact be much greater, since many of the causes of acute renal failure also are causes of increased breakdown of the tissues in general. The blood urea increases, the rate of increase being conditioned both by the degree of renal failure and by the amount of tissue breakdown. Besides nitrogen, the kidney can no longer excrete adequate amounts of water, sodium, and potassium.
These various inadequacies point the way to the necessary management of acute renal failure--the elimination from intake of any dangerous substance that the kidney can no longer handle. The diet must either be free of protein or contain small amounts of high-quality protein to lessen tissue breakdown. It must also be free from sodium and potassium: many persons with renal failure have died from pulmonary edema, a correlate of sodium retention, and others from the acute toxic effects on the heart of a raised level of potassium in the blood. Water cannot be excluded from the intake but must be limited to an amount estimated to equal the unavoidable loss of water from the skin and in breathing. The weight of the patient and the concentration of sodium in the blood are good guides to the adequacy of water restriction. In the absence of continuing losses of sodium from the body, as might occur from vomiting or diarrhea, a progressive fall in serum sodium implies that too much water is being taken in. Kidney function may recover, often in seven to 10 days. The use of dialysis, the removal of waste products by straining the blood through semipermeable membranes, gives further time for renal recovery. Potassium can be removed from the body by resins, but this is less often required if dialysis is available.
Although by comparison with the oliguric phase the recovery phase presents fewer problems, the convalescent kidney takes time to recover its full regulatory function, and electrolytes and water may be lost at an unusual rate during this stage, requiring replacement. Most individuals who survive completely recover from acute renal failure, but residual renal damage persists in some persons. In a few, this is so severe as to bring them effectively into the category of chronic renal failure. The artificial kidney has transformed the outlook for many patients with acute renal failure, and this, together with developments in the control of infection with more powerful antibiotics, constitutes one of the miracles of medicine in the last few decades.