Hepatitis: Kimmel PL

Cohen SD, Kimmel PL. · Division of Renal Diseases and Hypertension, Department of Medicine, George Washington University Medical Center, Washington, DC 20037, USA. · Semin Nephrol. · Pubmed #19013324 No free full text.

Abstract: Immune complex glomerulonephritis is a common diagnosis in renal biopsy series of human immunodeficiency virus (HIV)-infected patients. There are a variety of glomerulonephritides associated with HIV infection, including IgA nephropathy, membranoproliferative glomerulonephritis, membranous nephropathy, lupus-like glomerulonephritis, immunotactoid glomerulopathy, and fibrillary glomerulonephritis. In addition, HIV-related proteins may be implicated in circulating immune complexes directly related to a response to the infection. In some cases, the relationship of the HIV infection to the glomerulonephritis is unclear. HIV infection is associated with the development of polyclonal hypergammaglobulinemia, which can promote the development of circulating immune complexes. It is not clear if HIV-associated glomerulonephritis is caused by the passive trapping of these circulating immune complexes or the in situ deposition of antibodies binding to HIV viral antigens. Some renal lesions that are seen in the setting of HIV infection more likely may be related to the presence of a co-infection such as hepatitis C virus infection. The optimal therapy for immune complex glomerulonephritis in the setting of HIV infection is unknown. Because of the underlying immunosuppressed state of many HIV-infected patients, caution with traditional cytotoxic therapies is advised. The role of antiretroviral therapy in modifying the course of these renal lesions is unclear.

Cohen SD, Chawla LS, Kimmel PL. · Division of Nephrology, Department of Medicine, College of Physicians and Surgeons, Columbia University, Washington, District of Columbia, USA. · Curr Opin Crit Care. · Pubmed #19005305 No free full text.

Abstract: PURPOSE OF REVIEW: To present an overview of the epidemiology and etiology of acute kidney injury (AKI) in patients infected with human immunodeficiency virus (HIV). RECENT FINDINGS: HIV-infected patients are at an increased risk of developing AKI. Potential risk factors for the development of AKI in this patient population include increased HIV viral loads, reduced CD4 cell counts, hepatitis C virus coinfection, a history of diabetes, black race, male gender, and baseline chronic kidney and hepatic disease. Observational studies have found an increased morbidity and mortality in HIV-infected patients who develop AKI. There are diverse etiologies of AKI in HIV-infected patients, with increasing reports of highly active antiretroviral therapy-related nephropathy secondary to tenofovir nephrotoxicity. There have also been recent case reports of HIV-infected patients who develop a unique form of acute interstitial nephritis secondary to diffuse infiltrative lymphocytosis syndrome. SUMMARY: There are a variety of etiologies of AKI in HIV-infected patients. Prompt diagnosis and treatment of AKI is critical to help prevent morbidity and mortality in this patient population.

Jaffe JA, Kimmel PL. · Division of Renal Diseases and Hypertension, Department of Medicine, George Washington University Medical Center, 2150 Pennsylvania Avenue NW, Washington, DC 20037, USA. · Clin J Am Soc Nephrol. · Pubmed #17699270 links to  free full text

Abstract: 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 heroin-associated nephropathy, the evidence from in vitro cellular and animal studies to support the existence of cocaine-induced renal changes is more convincing.