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  • HIV-associated Nephropathy (HIVAN) is a distinct pathological entity characterized by the combination of collapsing FSGS, microcystic dilation of renal tubules, and interstitial inflammation found in HIV infected individuals

  • HIVAN is caused by expression of HIV-1 genes in renal epithelial cells and is highly associated with APOL1 risk alleles:

    • Combination antiretroviral therapy (cART) is the most effective treatment to retard progression of glomerular filtration decline and proteinuria:

      • Though cART protects against HIVAN, some individual agents are associated with a spectrum of renal manifestations from benign spurious changes in serum creatinine to fulminant acute kidney injury (AKI)

    • Small studies suggest a beneficial effect of angiotensin converting enzyme inhibitors and steroids in selected patients

  • HIV-positive patients are predisposed to AKI

  • HIV-associated immune complex kidney (HIVICK) disease includes a heterogeneous spectrum of glomerular diseases occurring in HIV-infected patients characterized by glomerular immune complex deposition

  • Thrombotic microangiopathy is an HIV-related complication most commonly found in patients with untreated/advanced HIV disease

  • HIV infection increases the risk of diabetic kidney disease progression, and may also promote progression of other common forms of chronic kidney disease (CKD).


General Considerations


At the onset of the HIV epidemic, little was known concerning the ability of the virus to cause end-organ damage. As treatment options evolved, so too, did the spectrum of kidney diseases caused by the virus. Initially, the lack of therapeutic options permitted the most severe of renal phenotypes, HIV-associated nephropathy (HIVAN), a clinical syndrome of nephrotic proteinuria and rapid renal function deterioration, to appear. The advent of combined antiretroviral therapy (cART) decreased the prevalence of fulminant HIVAN; however, its efficacy in treating other HIV-associated kidney complications including immune complex related disease, thrombotic microangiopathy (TMA), acute kidney injury (AKI), and synergy with other forms of glomerular disease are poorly defined. Though cART has markedly improved patient outcomes and reduced the incidence of end-stage renal disease (ESRD) due to HIVAN, several agents used in cART, can have nephrotoxic effects. In this chapter, we discuss the presentation, pathogenesis, and treatment of HIVAN, the prototypical HIV-induced kidney disease, as well as the spectrum of HIV-associated kidney diseases.



Razzak Chaudhary  S  et al: Trends in the outcomes of end-stage renal disease secondary to human immunodeficiency virus-associated nephropathy. Nephrol Dial Transplant 2015;30:1734.  [PubMed: 26175146]




In the United States, HIVAN occurs almost exclusively in persons of African descent. International studies evaluating HIV-infected patients with proteinuria corroborate the U.S. data. In fact, HIVAN has the strongest racial predisposition of any form of acquired renal disease leading to ESRD.


Recently, discoveries explain the genetic predisposition to HIVAN amongst persons of African descent. Polymorphisms in the gene for Apolipoprotein L1 (APOL1) explain the majority of excess race-attributed risk in blacks for non-diabetic ESRD. Patients with two copies of risk-associated APOL1 alleles, which provide protection ...

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