Renal Failure Renal failure results when the kidneys cannot remove the bodys metabolic wastes or perform

their regulatory functions. The substances normally eliminated in the urine accumulate in the body uids as a result of impaired renal excretion, leading to a disruption in endocrine and metabolic functions as well as uid, electrolyte, and acid base disturbances. ACUTE RENAL FAILURE Pathophysiology Acute renal failure (ARF) is a sudden and almost complete loss of kidney function (decreased GFR) over a period of hours to days. ARF manifests with oliguria, anuria, or normal urine volume. Oliguria (less than 400 mL/day of urine) is the most common clinical situation seen in ARF; Anuria (less than 50mL/day of urine) and normal urine Regardless of the volume of urine excreted, the patient with ARF experiences rising serum creatinine and BUN levels and retention of other metabolic waste products (azotemia) normally excreted by the kidneys. CATEGORIES OF ACUTE RENAL FAILURE Three major categories of conditions cause ARF: prerenal (hypoperfusion of kidney) intrarenal (actual damage to kidney tissue) postrenal (obstruction to urine ow). Prerenal conditions occur as a result of impaired blood ow that leads to hypoperfusion of the kidney and a drop in the GFR. Common clinical situations are volume-depletion states (hemorrhage or GI losses), impaired cardiac performance (myocardial infarction, heart failure, or cardiogenic shock),

and vasodilation (sepsis or anaphylaxis). Intrarenal causes of ARF are the result of actual parenchymal damage to the glomeruli or kidney tubules. Conditions such as burns, crush injuries, and infections, as well as nephrotoxic agents, may lead to acute tubular necrosis and cessation of renal function. With burns and crush injuries, myoglobin (a protein released from muscle when injury occurs) and haemoglobin are liberated, causing renal toxicity, ischemia, or both. Severe transfusion reactions may also cause intrarenal failure; hemoglobin is released through hemolysis, lters through the glomeruli, and becomes concentrated in the kidney tubules to such a degree that precipitation of hemoglobin occurs. Medications may also predispose a patient to intrarenal damage, especially nonsteroidal antiinammatory drugs (NSAIDs) and ACE inhibitors. These medications interfere with the normal autoregulatory mechanisms of the kidney and may cause hypoperfusion and eventual ischemia. Postrenal causes of ARF are usually the result of an obstruction somewhere distal to the kidney. Pressure rises in the kidney tubules; eventually, the GFR decreases. Although the exact pathogenesis of ARF and oliguria is not always known, many times there is a specic underlying problem. Some of the factors may be reversible if identied and treated promptly, before kidney function is impaired. This is true of the following conditions that reduce blood ow to the kidney and impair kidney function: (1) hypovolemia; (2) hypotension; (3) reduced cardiac output and heart failure; (4) obstruction of the kidney or lower urinary tract by tumor, blood clot, or kidney stone; and (5) bilateral obstruction of the renal arteries or veins. If these conditions are treated and corrected before the kidneysare

permanently damaged, the increased BUN and creatinine levels, oliguria, and other signs associated with ARF may be reversed. PHASES OF ACUTE RENAL FAILURE There are four clinical phases of ARF: initiation, oliguria, diuresis, and recovery. The initiation period begins with the initial insult and ends when oliguria develops. The oliguria period is accompanied by a rise in the serum concentration of substances usually excreted by the kidneys (urea, creatinine, uric acid, organic acids, and the intracellular cations [potassium and magnesium]). The minimum amount of urine needed to rid the body of normal metabolic waste products is 400 mL. In this phase uremic symptoms rst appear and lifethreatening conditions such as hyperkalemia develop. Some patients have decreased renal function with increasing nitrogen retention, yet actually excrete normal amounts of urine (2 L/day or more). This is the nonoliguric form of renal failure and occurs predominantly after nephrotoxic antibiotic agents are administered to the patient; it may occur with burns, traumatic injury, and the use of halogenated anesthetic agents.In the diuresis period, the third phase, the patient experiences gradually increasing urine output, which signals that glomerular ltration has started to recover. Laboratory values stop rising and eventually decrease. Although the volume of urinary output may reach normal or elevated levels, renal function may still be markedly abnormal. Because uremic symptoms may still be present, the need for expert medical and nursing management continues. The patient must be observed closely for dehydration during this phase; if dehydration occurs, the uremic symptoms are likely to increase. The recovery period signals the improvement of renal function and may take 3 to 12 months. Laboratory values return to the patients normal level. Although a permanent 1% to 3% reduction

in the GFR is common, it is not clinically signicant.