Abstract
Proteinuria is common in the setting of HIV infection, and may reflect comorbid kidney disease, treatment-related nephrotoxicity, and HIV-related glomerular diseases. The mechanisms of podocyte and tubulointerstial injury in HIV-associated nephropathy (HIVAN) have been the subject of intense investigation over the past four decades. The pathologic contributions of viral gene expression, dysregulated innate immune signaling, and ancestry-driven genetic risk modifiers have been explored in sophisticated cellular and whole animal models of disease. These studies provide evidence that injury-induced podocyte dedifferentiation, hyperplasia, cytoskeletal dysregulation, and apoptosis may cause the loss of glomerular filtration barrier integrity and slit diaphragm performance that facilitates proteinuria and tuft collapse in HIVAN. Although the incidence of HIVAN has declined with the introduction of antiretroviral therapy, the collapsing FSGS lesion has been observed in the context of other viral infections and chronic autoimmune disorders, and with the use of interferon-based therapies in genetically susceptible populations. This highlights the fact that the lesion is not specific to HIVAN and that the role of the immune system in aggravating podocyte injury warrants further exploration. This review will summarize our progress in characterizing the molecular mechanisms of podocyte dysfunction in HIVAN and other forms of HIV-associated kidney disease.
Highlights
In the four decades since the first cases of AIDS were reported in 1981, an estimated 77.5 million people have been infected with HIV and more than 34 million people have died from complications of HIV infection [1]
HIIV-associated nephropathy (HIVAN) quickly became the leading cause of end-stage kidney disease (ESKD) in people living with HIV (PLWH), demonstrating a marked predilection for individuals of African descent
The incidence of ESKD attributed to HIVAN plateaued in the United States following the widespread introduction of 3-drug antiretroviral therapy (ART) in 1997, HIVAN remains an important cause of kidney disease in the setting of untreated HIV infection [4]
Summary
Edited by: Ilse Sofia Daehn, Icahn School of Medicine at Mount Sinai, United States. North Shore Long Island Jewish Health System, United States Saraladevi Naicker, University of the Witwatersrand, South Africa. Specialty section: This article was submitted to Nephrology, a section of the journal
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