Indirect



Drugs that affect the systemic vascular resist­ance, the blood pressure, and/or the extracellular fluid volume may cause a decrease in renal blood flow and in the glomerular filtration rate. These hemodynamic changes can result in the devel­opment of prerenal azotemia. In individuals whose blood flow autoregulation is impaired and in those in whom the drug inhibits the autore-gulatory response of the kidney, the acute renal failure syndrome may evolve. Nonsteroidal anti­inflammatory drugs, as well as vasodilator drugs, may cause this type of renal injury.

Although less common, a postrenal or obstruc­tive pattern of renal injury is associated with a number of drugs. Retroperitioneal fibrosis and ob­structive nephropathy have been reported follow­ing the administration of methysergide and the beta-blocker practolol. Intratubular precipitation of crystals may result in acute renal dysfunction. Sulfonamide crystalluria was an important cause of renal dysfunction when the sulfa drugs were initially introduced. This drug-related renal dys­function is now rarely seen, as the newer sulfon­amides are more soluble. Acute renal failure may develop from intratubular precipitation of uric acid in patients receiving chemotherapy for can­cer. Renal dysfunction due to precipitation of ox­alic acid crystals within the renal tubule has been observed in patients ingesting ethylene glycol and occasionally in patients exposed to the anesthetic agent methoxyflurane.