Advances in the pathogenesis of HIV-associated kidney diseases.
Despite improved outcomes among persons living with HIV who are treated with antiretroviral therapy, they remain at increased risk for acute and chronic kidney diseases. Moreover, since HIV can infect renal epithelial cells, the kidney might serve as a viral reservoir that would need to be eradicated when attempting to achieve full virologic cure. In recent years, much progress has been made in elucidating the mechanism by which HIV infects renal epithelial cells and the viral and host factors that promote development of kidney disease. Polymorphisms in APOL1 confer markedly increased risk of HIV-associated nephropathy; however, the mechanism by which ApoL1 variants may promote kidney disease remains unclear. HIV-positive persons are at increased risk of acute kidney injury, which may be a result of a high burden of subclinical kidney disease and/or viral factors and frequent exposure to nephrotoxins. Despite the beneficial effect of antiretroviral therapy in preventing and treating HIVAN, and possibly other forms of kidney disease in persons living with HIV, some of these medications, including tenofovir, indinavir, and atazanavir can induce acute and/or chronic kidney injury via mitochondrial toxicity or intratubular crystallization. Further research is needed to better understand factors that contribute to acute and chronic kidney injury in HIV-positive patients and to develop more effective strategies to prevent and treat kidney disease in this vulnerable population.
Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Michael J
MJ
Ross
D016263:AIDS-Associated Nephropathy / Q000209:etiology*; D058186:Acute Kidney Injury / Q000209:etiology; D019380:Anti-HIV Agents / Q000009:adverse effects; D000075944:Apolipoprotein L1; D001053:Apolipoproteins / Q000235:genetics; D005814:Genes, Viral; D020022:Genetic Predisposition to Disease; D015497:HIV-1 / Q000235:genetics / Q000472:pathogenicity; D006801:Humans; D007105:Immune Complex Diseases / Q000209:etiology; D007684:Kidney Tubules / Q000293:injuries / Q000821:virology; D008075:Lipoproteins, HDL / Q000235:genetics; D008954:Models, Biological; D050199:Podocytes / Q000473:pathology / Q000821:virology; D011110:Polymorphism, Genetic; D012307:Risk Factors; D057049:Thrombotic Microangiopathies / Q000209:etiology
C108666:APOL1 protein, human; D019380:Anti-HIV Agents; D000075944:Apolipoprotein L1; D001053:Apolipoproteins; D008075:Lipoproteins, HDL