Kidney damage in HIV infection: pathogenetic aspects, clinical and morphological variants and the role of antiretroviral therapy

Abstract

The review analyzes the prevalence and pathogenetic aspects of HIV infection. The main clinical and morphological variants of kidney damage in HIV infection are outlined. The prevalence of kidney damage in HIV infection is 20–30%, which are represented by such clinical and morphological variants as HIV-associated nephropathy (VAN), immunocomplex HIV-associated kidney disease, and thrombotic microangiopathy. In patients with HIV infection who are not treated with antiretroviral therapy (ART) the most common type of kidney disease is HIVAT. A decrease in the number of CD4+ cells, high viral load, advanced age, and the presence of kidney pathology in the next of kin are risk factors for the development of HIVAT. Specific risk factors for kidney damage in HIV infection are the use of antiretroviral drugs (tenofovir), the uncontrolled use of which is accompanied by tubular dysfunction. In HIV infection, the degree of immunodeficiency correlates with the severity of kidney damage. The most common histopathological manifestations of kidney damage in individuals with HIV infection are focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis, immunoglobulin A nephropathy, and mesangioproliferative glomerulonephritis. Hypertension, nephrotic syndrome, and reduced CD4+ cells are predictive of renal failure in HIV infection. In patients with HIV infection who are treated with ART the appearance of hypokalemia, nocturia, polyuria, microhematuria, and/or subnephrotic proteinuria is indicative of tubulointerstitial disease. To assess the total filtration function of the kidneys in people with HIV infection, the most acceptable formula is CKD-EPI.