Figure 733

Possible pathogenic mechanisms of glomerulosclerosis associated with HIV infection. HIV-associated glomerulosclerosis is not the result of opportunistic infections. Indeed, the nephropathy may be the first manifestation of HIV infection and often occurs in patients before opportunistic infections develop. HIV-associated glomeru-losclerosis also is not an immune-complex-mediated glomerulopathy because immune deposits are generally absent. Three mechanisms have been proposed: direct injury of renal epithelial cells by infective HIV, although direct renal cell infection has not been demonstrated conclusively and systematically; injury by HIV gene products; or injury by cytokines and growth factors released by infected lymphocytes and monocytes systemically or intrarenally or released by renal cells after uptake of viral gene products. The variable susceptibility to glomerulosclerosis also suggests that unique viral-host interactions may be necessary for expression of the nephropathy [132,156,166,173-175].

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