HIV-associated Nephropathy
This chapter provides information on histology, epidemiology, pathogenesis, genetic factors, and treatment associated with HIV-associated nephropathy, or HIVAN. In classic HIVAN, the kidneys are enlarged or normal in size on gross examination, consistent with the histologic findings of glomerular and tubular epithelial proliferation. The glomerular lesion of HIVAN is a collapsing form of focal segmental glomerulosclerosis (FSGS), characterized by podocyte proliferation and dedifferentiation. Renal tissue from patients with idiopathic or HIV-associated collapsing FSGS demonstrates loss of podocyte maturity markers, including synaptopodin, podocalyxin, and the Wilms' tumor antigen WT-1. The predilection of HIVAN for seropositive patients of African descent suggests that host genetic factors play an important role in the pathogenesis of HIVAN. Expression of HIV-1 mRNA in tubular epithelial cells can be detected throughout the renal tubule in biopsies from patients with HIVAN. The pattern of viral mRNA expression is similar to the development of tubular microcysts, consistent with a pathogenic role for viral infection. There are currently no randomized clinical trial data to guide the treatment of HIVAN. Limited observational data have suggested a potential role for corticosteroids and inhibitors of the renin-angiotensin-aldosterone system. The rationale for use of corticosteroids in HIVAN is extrapolated from limited data in other renal diseases with overlapping clinical or histologic features, including hepatitis C virus-related membranoproliferative glomerulonephritis and idiopathic FSGS. In addition, corticosteroids have been hypothesized to ameliorate the inflammatory interstitial component of HIVAN. The established benefit of ACE inhibitors in other proteinuric renal diseases formed the basis for their initial use in HIVAN. © 2009 Elsevier Inc. All rights reserved.
