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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 (HIVAN), a type of nephrotic syndrome (see Overview of Nephrotic Syndrome) seems to be more common among black patients with HIV who are injection drug users or have been poorly compliant with antiretroviral therapy. Infection of renal cells with HIV may contribute.
Most clinical findings are similar to those of focal segmental glomerulosclerosis (see Focal Segmental Glomerulosclerosis : Symptoms and Signs), but hypertension is less common and the kidneys remain enlarged. Most patients experience rapid progression to end-stage renal disease within 1 to 4 mo.
HIVAN is suspected in patients with nephrotic syndrome or nephropathy who have AIDS or symptoms of AIDS. HIVAN 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).
In HIVAN, 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 SLE, are found within endothelial cells but are now rare with more effective HIV therapy. Normotension and persistently enlarged kidneys help to differentiate HIVAN from focal segmental glomerulosclerosis.
Control of the HIV infection may help minimize renal damage. ACE inhibitors are probably of some benefit. The role of corticosteroids is not well defined. Dialysis is usually required. At some centers, outcomes after transplantation have been excellent.
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