The two most common HIV-associated renal diseases, HIV-associated nephropathy and HIV-immune-complex kidney disease, share the common pathologic finding of hyperplasia within the glomerulus. Podocyte injury is central to the pathogenesis of these diseases; however, the source of the proliferating glomerular epithelial cell remains a topic of debate. Parenchymal injury has been linked to direct infection of renal epithelial cells by HIV-1, although the mechanism of viral entry into this non-lymphoid compartment is unclear. Although transgenic rodent models have provided insight into viral proteins responsible for inducing renal disease, such models have important limitations. Rodent HIV-1 models, for instance, cannot replicate all aspects of immune activation, a process that could have an important role in the pathogenesis
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