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Renal disease in cocaine and heroin users is associated with the nephrotic syndrome, acute glomerulonephritis, amyloidosis,
interstitial nephritis, and rhabdomyolysis. The pathophysiologic basis of cocaine-related renal injury involves renal hemodynamic
changes, glomerular matrix synthesis and degradation, and oxidative stress and induction of renal atherogenesis.
Heroin is the most commonly abused opiate in the United States. Previous studies identified a spectrum of renal diseases in
heroin users. The predominant renal lesion in black heroin users is focal segmental glomerulosclerosis and in white heroin
users is membranoproliferative glomerulonephritis. Although the prevalence of heroin use in the United States has increased,
the incidence of “heroin nephropathy” has declined. Because reports of heroin nephropathy predated the surveillance of
hepatitis C virus and HIV, the varied findings might be related to the spectrum of viral illnesses that are encountered in
injection drug users. Socioeconomic conditions, cultural and behavioral practices, or differences in genetic susceptibilities
may be more associated with the development of nephropathy in heroin users than the drug’s pharmacologic properties.
Administration of cocaine in animal models results in nonspecific glomerular, interstitial, and tubular cell lesions, but there
is no animal model of heroin-associated renal disease. The heterogeneity of responses that are associated with heroin is not
consistent with a single or simple notion of nephropathogenesis. There are no well-designed, prospective, epidemiologic
studies to assess the incidence and the prevalence of renal disease in populations of opiate users and to establish the validity
of a syndrome such as heroin nephropathy. It is concluded although there is a paucity of evidence to support a heroinassociated
nephropathy, the evidence from in vitro cellular and animal studies to support the existence of cocaine-induced
renal changes is more convincing.
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