Clinical Pearls & Morning Reports
The spectrum of human immunodeficiency virus (HIV)-associated renal diseases includes conditions that are directly associated with infection, those that are linked to the systemic immune response to infection, those that develop as a consequence of superinfections, and those that are associated with the treatment of HIV infection. Over the past two decades, antiretroviral therapy has converted HIV infection to a chronic illness, with associated changes in the incidence, type, and severity of HIV-associated kidney diseases. Read the latest Review Article.
Q: How has antiretroviral therapy affected the incidence and prevalence of end-stage renal disease in patients with HIV infection?
A: Over the past 20 years, the incidence of end-stage renal disease attributed to HIV infection has declined and then plateaued, whereas the prevalence of end-stage renal disease in persons with HIV infection continues to increase, because patients live longer with effective antiretroviral therapy.
Q: What are some of the features of HIV-associated nephropathy?
A: HIV-associated nephropathy affects all renal tissue compartments, including glomeruli, tubules, and interstitium. A collapsing form of focal segmental glomerulosclerosis is a typical manifestation of HIV-associated nephropathy. In the United States, HIV-associated nephropathy occurs primarily in persons of African descent, particularly in those with markedly reduced CD4 counts and elevated viral loads. The genetic predisposition to HIV-associated nephropathy among patients of African descent is due largely to variants in the APOL1 gene, encoding apolipoprotein L1. The prevalence of HIV-associated nephropathy has decreased dramatically since the introduction of antiretroviral therapy and consequent effective suppression of viral replication.
A: Although it is likely that selection bias is a factor in renal-biopsy registries, HIV immune-mediated kidney disease has become the most common histopathological diagnosis in several studies of biopsy specimens from HIV-infected patients. The reasons underlying the increasing relative prevalence of HIV immune-mediated kidney disease are unknown but may reflect modulation of the immune system induced by antiretroviral therapy, which can lead to immune reconstitution and immune-complex deposition, or it could be due to the decline in the incidence of HIV-associated nephropathy. Types of HIV immune-mediated kidney disease include diverse renal histologic manifestations — HIV-associated IgA nephropathy, postinfectious glomerulonephritis, lupus-like glomerulonephritis, membranoproliferative glomerulonephritis, cryoglobulinemic glomerulonephritis, mesangial proliferative glomerulonephritis, membranous nephropathy, and other conditions that are usually characterized by glomerular hypercellularity, inflammation, and varying degrees of fibrosis and scarring. Thrombotic microangiopathy is another cause of renal disease associated with HIV infection. HIV has indirect cytopathic effects that precipitate endothelial injury, leading to thrombotic microangiopathy. Antiretroviral therapy can be associated with nephrotoxic effects, including acute and chronic renal disease. Tenofovir disoproxil fumarate can cause renal tubular dysfunction, which leads to Fanconi’s syndrome, nephrogenic diabetes insipidus, acute tubular necrosis, and ultimately chronic kidney disease.
A: Although the incidence of HIV-associated end-stage renal disease has plateaued, the prevalence of HIV-infected patients undergoing dialysis in the United States continues to increase. Survival among patients with HIV infection who undergo dialysis is similar to that among patients without HIV infection who undergo dialysis. Survival among HIV-infected patients does not differ between those who undergo peritoneal dialysis and those who undergo hemodialysis. A dramatic advance in the care of patients with HIV-associated end-stage renal disease occurred after kidney transplantation was shown to be viable. Although the rates of acute rejection are higher among HIV-infected transplant recipients than among other kidney transplant recipients, outcomes with respect to patient and allograft survival are similar.