HIV-associated nephropathy is characterized by clinical findings similar to those of focal segmental glomerulosclerosis and often biopsy features of collapsing glomerulopathy (a variant of focal segmental glomerulosclerosis).
HIV-associated nephropathy, a type of nephrotic syndrome, seems to be more common among Black patients with HIV who are injection drug users or have been poorly adherent to their antiretroviral therapy regimen. Infection of renal cells with HIV may contribute.
Most clinical findings are similar to those of focal segmental glomerulosclerosis, but hypertension is less common and the kidneys remain enlarged.
Most patients experience rapid progression to end-stage kidney disease within 1 to 4 months.
Diagnosis of HIV-Associated Nephropathy
Renal biopsy
HIV-associated nephropathy is suspected in patients with nephrotic syndrome or nephropathy who have AIDS or symptoms of AIDS. HIV-associated nephropathy should be distinguished from the many other disorders that occur with higher frequency in HIV-infected patients and cause renal disease, such as thrombotic microangiopathy (hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura), immune complex–mediated glomerulonephritis, and drug-induced interstitial nephritis (due to indinavir and ritonavir) and rhabdomyolysis (due to statins).
Ultrasonography, if done, shows that the kidneys are enlarged and highly echogenic.
Renal biopsy typically is done. Light microscopy shows capillary collapse of varying severity (collapsing glomerulopathy) and differing degrees of increased mesangial matrix. Tubular cells show marked degenerative changes and tubular atrophy or microcytic dilation. Interstitial immune cell infiltrate, fibrosis, and edema are common. Tubular reticular inclusions, similar to those in systemic lupus erythematosus, are found within endothelial cells but are now rare with more effective HIV therapy.
Focal segmental glomerulosclerosis with collapse of glomerular tufts and microcystic tubular changes is characteristic of HIV-associated nephropathy (Jones silver stain, ×100).
Image provided by Agnes Fogo, MD, and the American Journal of Kidney Diseases' Atlas of Renal Pathology (see www.ajkd.org).
HIV-associated nephropathy can be distinguished from focal segmental glomerulosclerosis by reticular inclusions in endothelial cell cytoplasm on transmission electron microscopy (×20,000). However, these reticular inclusions are now rare with use of highly active antiretroviral therapy.
Image provided by Agnes Fogo, MD, and the American Journal of Kidney Diseases' Atlas of Renal Pathology (see www.ajkd.org).
Focal segmental glomerulosclerosis with collapse of glomerular tufts and microcystic tubular changes is characteristic of HIV-associated nephropathy (Jones silver stain, ×100).
Image provided by Agnes Fogo, MD, and the American Journal of Kidney Diseases' Atlas of Renal Pathology (see www.ajkd.org).
HIV-associated nephropathy can be distinguished from focal segmental glomerulosclerosis by reticular inclusions in endothelial cell cytoplasm on transmission electron microscopy (×20,000). However, these reticular inclusions are now rare with use of highly active antiretroviral therapy.
Image provided by Agnes Fogo, MD, and the American Journal of Kidney Diseases' Atlas of Renal Pathology (see www.ajkd.org).
Normotension and persistently enlarged kidneys help to differentiate HIV-associated nephropathy from focal segmental glomerulosclerosis.
Treatment of HIV-Associated Nephropathy
Antiretroviral therapy (ART) and angiotensin inhibition
Control of the HIV infection may help minimize renal damage; in fact, HIV-associated nephropathy is rare in patients taking ART with well-controlled HIV infection. Angiotensin inhibition with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) is probably of some benefit. The role of corticosteroids is not well defined. At some centers, outcomes after kidney transplantation have been excellent.
