Induced Kidney Disease

See Chapter 49, Drug-Induced Kidney Disease, authored hy Thomas D. Nolin and Jonathan Himmelfarb, for a more detailed discussion of this topic. 

Wedeen RP, Qian L. 1991. Chromium-induced kidney disease. Environ Health Perspect 92 71-74. 

Pearson J (2008) Drug-induced kidney disease. In Ashley C, Morlidge C (eds) Introduction to Renal Therapeutics. London Pharmaceutical Press, 139-144. 

Duggin GG. Combination analgesic-induced kidney disease the Australian experience. Am J Kidney Dis 1996 28 (suppi 1) S39-S47. 

Pommer W. Clinical presentation of analgesic-induced nephropathy. In Analgesic and NSAID-induced kidney disease. Stewart JH (editor). Oxford University Press, Oxford 1993 p. 108-118. 

The initial diagnosis of drug-induced kidney disease typically involves detection of elevated serum creatinine and blood urea nitrogen, for which there is a temporal relationship between the toxicity and use of a potentially nephrotoxic drug. 

Mechanisms of drug-induced kidney disease include immune-mediated toxicities (e.g., glomerulonephritis and allergic interstitial nephritis) and nonimmunologic-mediated toxicities which effect specialized characteristics of normal renal physiology. 

Drug-induced kidney disease is best prevented by avoiding the use of potentially nephrotoxic agents in patients at increased risk for toxicity. However, when exposure to these drugs cannot be avoided, recognition of risk factors and specific techniques such as hydration may be used to reduce potential nephrotoxicity. 

Acute tubular necrosis is the most common presentation of drug-induced kidney disease in hospitalized patients. The primary agents implicated are aminoglycosides, radiocontrast media, cisplatin, amphotericin B, foscarnet, and os-motically active agents. 

Health effects are not occurring among exposed workers by determining B2MU as an early indicator of the onset of cadmium-induced kidney disease. 

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