Abstract
HIV-1 associated nephropathy is a rapidly progressive form of focal segmental glomerulosclerosis typically seen in patients of African ancestry. HIV-transgenic mice can develop an HIVAN-like renal disease. Zhong et al. show that the oral administration of a cyclic nucleotide phosphodiesterase 4 inhibitor and a retinoic acid receptor-alpha agonist can prevent the development of HIVAN in transgenic mice, acting through a cAMP dependent mechanism that is independent of HIV-1 genes. These findings suggest that endogenous host factors play a critical role in HIVAN.
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