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Both diagnostic and therapeutic studies frequently utilize radiocontrast media to enhance images. As a result, use of these agents has increased markedly over the past decade with more than 10 million studies performed on a yearly basis in the United States. Development of acute kidney injury (AKI) is a common complication of radiocontrast exposure in patients who possess underlying risk factors. Impor-tantly, radiocontrast-induce nephropathy (RCIN) is associated with increased short- and long-term mortality. Thus, at risk patients should be identified prior to administration of radiocontrast to allow choice of other potential imaging options or employment of prophylactic interventions. Currently, use of isotonic intravenous fluids is the only proven beneficial preventive therapy. Use of low volumes of radiocontrast and avoidance of nephrotoxic medications are also accepted as nephroprotective. Mixed results exist on the utility of N-acetylcysteine (NAC) therapy and low versus iso-osmolar radiocontrast agents in preventing RCIN. While hemodialysis appears to have no beneficial role, a single center's experience with hemofiltration is associated with a reduction in RCIN and other clinical endpoints. Several therapies have no role in the prevention of RCIN and should be avoided. This review will provide an up to date examination of the current status of these issues as they relate to RCIN.

Conventional nonsteroidal anti-inflammatory drugs (NSAIDs), i.e. nonselective cyclooxygenase COX inhibitors have well-documented nephrotoxicity. Adverse renal effects occur because of inhibition of the synthesis of cyclooxygenase-derived prostaglandins which act to modulate pathologic processes that would normally impair various renal functions. The introduction of the selective COX-2 inhibitors raised hope that this class of drugs would reduce injury in both the gastrointestinal tract and the kidneys. Animal and human data, however, suggest that COX-2 synthesized prostaglandins are important in the modulation of renal physiology during adverse conditions. Hence, it appears that these drugs are equal in causing nephrotoxicity as the nonselective COX inhibitors.

Acute renal failure is a well-described renal syndrome observed in patients infected with the human immunodeficiency virus (HIV). Underlying glomerular disease and disturbances in renal tubular function predispose these patients to a number of hemodynamic and nephrotoxic insults. Prerenal azotemia from both "true" and "effective" depletion of intravascular volume is the most common cause of acute renal insufficiency in patients infected with HIV. Direct damage to the renal tubules from both nephrotoxic medications and prolonged ischemic processes occurs frequently in hospitalized patients. Injury to the tubulointerstitium of the kidney may also result from allergic reactions to medications prescribed to patients. Deposition of crystals in the tubular lumens, and rarely in the glomerular capillaries, will cause acute renal failure in the setting of tumor lysis syndrome or during therapy with medications associated with crystal nephropathy. Finally, obstruction of the urinary system will rarely cause postrenal azotemia in patients infected with HIV.

Several medications--notably acyclovir, sulfonamides, methotrexate, indinavir, and triamterene--are associated with the production of crystals that are insoluble in human urine. Intratubular precipitation of these crystals can lead to acute renal insufficiency. Many patients who require treatment with these medications have additional risk factors, such as true or effective intravascular volume depletion and underlying renal insufficiency, that increase the likelihood of drug-induced intrarenal crystal deposition. Acute renal failure in this setting may be preventable if it is anticipated by appropriate drug dosing, volume expansion with high urinary flow, and alkalinization of the urine when appropriate. Renal failure may be reversible if the drug is discontinued, and by volume repletion and alkalinization of the urine when appropriate. Management of established renal insufficiency includes volume repletion, dialytic support if necessary, adjustment of drug doses, and avoidance of further exposure to nephrotoxins.

Phosphate intoxication, manifested by hypocalcemic tetany and acute renal failure, may complicate bowel-cleansing preparations which contain phosphate. These preparations are commonly used to prepare patients for various gastrointestinal procedures. Often, patients who receive these regimens are at increased risk of phosphate intoxication from diseases which slow gastrointestinal transit or decrease renal excretion (renal insufficiency). We present a patient who developed oliguric acute renal failure from severe phosphate intoxication associated with a phosphate-containing bowel-cleansing regimen.

Intravenous immune globulin (IVIG) therapy has been used more commonly to treat a number of clinical disorders. During the past 10 years, IVIG infusion has been associated with a variety of complications. Acute renal failure, which was not described in the initial drug trials, was recognized as an adverse effect of IVIG therapy in 1987. Since the original report, a number of cases have been described in the literature. Older age and preexisting renal impairment appear to predispose to the development of acute renal failure. Acute renal insufficiency develops within days and resolves over several days to weeks. However, in some cases, recovery is delayed and initiation of renal replacement therapy is required. Chronic renal insufficiency requiring maintenance dialysis is extremely rare. The precise cause of IVIG-associated acute renal failure is unknown but may be attributable to either the direct effects of the immunoglobulin or the stabilizing agent used in the IVIG preparation.

Over the past decade, intravenous immune globulin therapy (IVIG) has gained widespread use for a variety of clinical disorders. IVIG treatment is associated with a number of complications, including acute renal failure (ARF). Although the cause of IVIG-associated ARF is unknown, it may be related to the stabilizing agent used in the IVIG preparation. The development and resolution of ARF is typically rapid, but is some cases recovery may be delayed and require renal replacement therapy. In such patients, recurrence of ARF may be avoided by selection of a preparation with a different stabilizing agent. Two cases of IVIG-induced ARF are described, and all reported cases are analyzed to assess the probable mechanism of renal injury.

Acute renal failure (ARF) is a relatively frequent complication associated with heart transplantation. It develops in the first few days postoperatively and is characterized by oliguria with laboratory and urinary indices typical of pre-renal azotemia. Cyclosporine, especially with higher doses, is one of the many factors which play an integral part in the nephrotoxicity following cardiac transplant. Poor preoperative renal function and perioperative hemodynamic compromise may also contribute to ARF. The actual incidence of ARF now encountered by transplant centers may be lower than previously reported, the result of lower cyclosporine doses. Currently, management is entirely supportive, but novel therapeutic approaches with atrial natriuretic peptide-like substances are being explored. A case illustrating the typical clinical presentation of ARF after heart transplant will be presented and the clinical features will be reviewed.

The success of ketorolac as a nonnarcotic analgesic is likely to propagate its widespread use to control moderate to severe postoperative pain. Indeed, of the patients treated with ketorolac and described in the medical literature, nearly 90% had had a major surgical procedure. Since any such procedure may be associated with significant third-spacing of the fluid and result in renal hypoperfusion, care must be taken in administering ketorolac. Close attention to urine output and parameters of renal function must be maintained. Moreover, postoperative ketorolac therapy should be avoided in patients who have conditions that predispose to NSAID nephrotoxicity (as in our Case 1). Likewise, in nonsurgical patients the same degree of caution should be used with ketorolac as with any oral NSAID. Finally, since ketorolac is excreted almost entirely by the kidney, either elderly patients or patients with underlying renal insufficiency must have an adjustment of the dosing interval, or this medication should be avoided in such patients altogether.