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Dr. Bruggemans current affiliation: Rammelkamp Center for Research and Education, Case Western Reserve University, Cleveland, Ohio.
Division of NephrologyMount Sinai School of Medicine, New York, New York.
Correspondence to Dr. Michael J. Ross, One Gustave L. Levy Place, Box 1243, New York, NY 10029. Phone: 212-241-0131; Fax: 212-987-0389; E-mail: michael.ross{at}mssm.edu
ABSTRACT. Tubular microcyst formation is a prominent histopathologic feature of HIV-associated nephropathy (HIVAN), but its pathogenesis is unknown. HIV-1 has recently been shown to infect renal tubular epithelial cells in patients with HIVAN. In addition, HIV-1 gene expression in renal epithelial cells has been shown to cause a renal disease that is identical to HIVAN in HIV-1 transgenic mice. In these studies, immunohistochemistry for tubular segment-specific markers and mRNA in situ hybridization for HIV-1 was used to determine which tubular segments develop microcysts and which segments express HIV-1 in the kidneys of transgenic mice and patients with HIVAN. It was found that microcysts involve multiple nephron segments in both patients with HIVAN and HIV-1 transgenic mice. Furthermore, HIV-1 infection in HIVAN and HIV-1 transgene expression also occurs in multiple segments of the nephron. These data support a direct role for HIV-1 infection of renal epithelial cells in the pathogenesis of microcyst formation in patients with HIVAN.
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