Pathogenesis of human immunodeficiency virus (HIV)-associated nephropathy

Semin Nephrol. 1998 Jul;18(4):436-45.

Abstract

Human immunodeficiency virus-associated nephropathy (HIVAN) is the third leading cause of end-stage renal failure in Blacks between the ages of 20 and 64. Because the incidence of HIV infection has continued to increase in Blacks as survival has improved, the pool of patients alive and at risk for developing HIVAN has vastly expanded. This suggests that HIVAN will continue to increase in importance to the end-stage renal disease program. The racial predilection for the disease in Blacks implies that genetic or environmental cofactors are involved. Evidence in human and animal models has shown that proliferation of renal epithelial cells is the predominant feature of the disease and that apoptosis occurs. The prospect that renal infection is necessary to stimulate cells to proliferate remains a possibility but is not yet proven. Cytokine dysregulation may also be involved in disease progression, but evidence is lacking that altered cytokine production is the proximate cause of HIVAN. Many issues remain to be resolved including the potential for renal infection in vivo, the mechanisms responsible for proliferation and apoptosis, and factors that provide racial susceptibility to HIVAN. Advances in our understanding of pathogenesis will be required to control the growth of HIV-related renal diseases in the ESRD population.

Publication types

  • Review

MeSH terms

  • AIDS-Associated Nephropathy / pathology
  • AIDS-Associated Nephropathy / physiopathology*
  • Animals
  • Apoptosis
  • Cats
  • Diagnosis, Differential
  • Disease Models, Animal
  • Disease Progression
  • HIV-1 / immunology*
  • Humans
  • Kidney / immunology
  • Kidney / pathology
  • Mice
  • Mice, Transgenic