الفهرس 
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Abstract
Medications cause renal disease by promoting various types of injury in the kidney. Several drugs reduce renal perfusion and cause prerenal azotemia. Vascular disease can develop following exposure to various medications through direct and indirect effects. A number of glomerular lesions have been described with therapeutic agents and illicit drugs. Acute interstitial nephritis occurs from a drug-induced allergic reaction, which promotes interstitial inflammation and tubular damage. Acute tubular necrosis is a dose-dependent process that occurs from direct drug toxicity on tubular epithelia. Other less common patterns of drug-induced tubular injury include osmotic nephropathy, crystal nephropathy and acute nephrocalcinosis, finally, postrena! azotemia from structural or functional obstruction of the urinary tract also complicates therapy with a number of medications.
Therpaeutic agents are a relatively frequent cause of kidney disease. Prerenal azotemia commonly develops in at risk patients treated with NSAIDs, selective COX-2 inhibitors and calcineurin inhibitors. The renal parenchyma is another common target of drugs. Vascular disease develosp from a number of medications, which can cause thrombotic microangio-pathy with associated vascular occlusion and glomerular ischemia. Several drugs may incite an allergic reaction within the kidney leading to intetstitial inflammation and tubular damage. This idiosyncratic pattern of renal injury is referred to as AIN is often noted following exposure to (B-lactam antibiotics and sulfonamide,s but can be seen with NSAIDs, selective Cox-2 inhibitors, and the protease inhibtiro atazanavir. ATN is probably the most common kidney lesion that develosp int eh setting of drug therapy. It is a dose dependent process characterized by a direct toxic effect on tubular epithelia. Tubular damage may also reustl from other less well recognized drug effects including osmotic nephropathy and crystal nephropathy. Osmotic nephropathy occurs from the osmolar properties of medications such as IVIG (from the sucrose stabilizer) and HES. Crystal nephropathy, whereby therapeutic agents and their derivatives precipitate in distal tubules, leading to obstruction and renal failure, develosp from several drugs including sulfadiazine and indinavir. Bilateral obstruction of the urinary tract (or unilateral obstruction in a single functioning kidney) from drug induced calculi may cause postrenal azotemia. Drug induced aetiology should be considered in all forms o fkidney disease. Careful attention to the time course of adverse events and diligent clinical pathological correlation may provide insight into new and important patterns of drug induced nephrotoxicity.