Kidney is one of the organs, as haematopoietic tissue and central nervous system, representing a reservoir of HIV-1, where the virus can exert a direct pathogenic activity. HIV-associated nephropathy (HIVAN) is the prominent illness among the numerous renal injuries occurring in HIV-1 infection. It is characterized by heavy proteinuria and rapid progression to end stage renal disease. Histopathologically, HIVAN is a collapsing form of focal segmental glomerulosclerosis with podocyte hyperplasia and dedifferentiation, associated with severe tubulopathy which is characterized by tubular apoptosis, microcysts, and interstitial fibrosis. Several clinical and experimental data point to a direct role of HIV-1 in kidney damage. In renal biopsies of HIVAN cases viral transcripts have been found in glomerular and tubular epithelial cells. Transgenic mice expressing replication-defective HIV proviral constructs develop a renal disease similar to HIVAN both from the histopathological and clinical point of view. In vitro studies using cultures of human renal cells have shown that HIV-1 can induce in glomerular and tubular cells distinct pathogenic effects, which mimic the pathological features of HIVAN in vivo. A large body of evidence suggests that an abnormal response of podocytes to HIV-1 infection and/or HIV-1 proteins is the key event in HIVAN pathogenesis. Since the highly-active antiretroviral therapy has demonstrated scant beneficial effects on the development of HIVAN, the elucidation of the pathogenic mechanisms activated by HIV-1 in the renal cells might allow designing specific therapeutic strategies.
|Translated title of the contribution||HIV-1 and renal cells: pathogenesis of HIV-associated nephropathy|
|Number of pages||12|
|Journal||Giornale italiano di nefrologia : organo ufficiale della Società italiana di nefrologia|
|Publication status||Published - Nov 2005|
ASJC Scopus subject areas