Nonsteroidal anti-inflammatory drugs(NSAIDs) have several acute renal effects. NSAIDs are potent inhibitors of prostaglandin synthesis, a property that contributes their nephrotoxic potential in certain high-risk patients in whom renal vasodilatation depends on prostaglandins.
The most frequent pattern of injury related to NSAIDs is prerenal azotemia, particularly in patients who either are volume contracted or have a reduced effective circulating volume.
Susceptible persons include those with congestive heart failure, cirrhosis, chronic renal disease, and volume depletion. Hyperchloremic metabolic acidosis, often associated with hyperkalemia, has also been recognized as an effect of the NSAIDs, particularly in persons with preexisting chronic interstitial renal diease. Hypireninemic hypoaldosteronism occurs in these persons in states of renal prostaglandin inhibition. Finally, NSAIDs have been associated with the development of acute interstitial nephritis, often associated with renal insufficiency and nephrotic-range proteinuria. This complication appears to be an idiosyncratic reaction to propionic acid derivatives such as ibuprofen, naproxen, and fenprofen. In contrast to acute interstitial nephritis associated with other drugs, the incidence of hypersensitivity symptoms and eosinophilia is low. Discontinuation of the offending agent usually results in resolution of this disorder. Renal injury is a well-recognized and dose-dependent complication of cisplatin use in the management of many carcinomas. Hypomagnesemia resulting from renal losses of magnesium may be severe and can occur in as many as 50% of patients.
Patients should be well hydrated before they receive cisplatin, and known nephrotoxins should be avoided whenever possible. The usual lesion is that of ATN, but with severe damage or recurrent administration of the drug, chronic interstitial disease may ensue. Ingestion of ethylene glycol, usually in the form of antifreeze, produces a characteristic rome of a severe union gap metabolic acidosis and a large osmolal gap.
ARF generally manifests after 48 to 72 hours. Patients are disoriented and agitated initially, and they progress central nervous system depression, stupor, and coma. Cardiovascular collapse and death then follow.