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is of particular concern and must be treated with life-long prophylaxis to prevent fatal
recurrence. A negative urine bacterial culture should prompt search for fungal agents such as
Candida, viral agents such as cytomegalovirus, or mycobacteria. Lower UTI may ascend to
cause pyelonephritis, and gram negative bacteria are the most likely agents. Opportunistic
agents leading to pyelonephritis with HIV infection can include Candida, Mycobacteria,
Histoplasma, and Pneumocystis. Mycobacterial infections typically start in the kidney from
hematogenous spread, then descend the urinary tract.[919,923]
Acute renal failure from prerenal causes can occur from volume depletion with fluid loss
from vomiting or diarrhea. Sepsis can lead to volume depletion with similar outcome. Renal
diseases leading to serious morbidity and mortality with AIDS can be seen in both early and late
stages. Both acute renal failure as well as end stage renal disease can occur. Though not
common, end stage renal disease may result from varied etiologies, including HIV
nephropathy.[922]
Additional pathologic findings in HIV-infected persons include arterionephrosclerosis,
glomerulonephritis (most often with a membranoproliferative pattern), pyelonephritis, interstitial
nephritis, diabetic nephropathy, fungal infection, and amyloidosis. The variety of lesions
increases with prolonged survival and increasing prevalence of diabetes mellitus and
hypertension.[924]

HIV NEPHROPATHY.-- The kidney may show a so-called "HIV-associated
nephropathy" (HIVAN), or HIV nephropathy (HIVN). About 50% of persons developing
HIVAN have a history of injection drug use. In over 90% of cases the affected person is Black,
though a few are Hispanic, and the disease is rare in Caucasians. There is direct infection of
renal epithelial cells by HIV. Persons susceptible to HIVAN may have a mutation in the
podocyte-expressed nonmuscle myosin heavy chain 9 (MYH9).[925] In addition, the podocyte
host response to HIV-1 includes down-regulation of MYH9 expression that may contribute to the
pathogenesis of HIVAN.[926]
HIVAN is characterized by marked proteinuria and a rapid progression to renal failure
and end stage renal disease (ERSD). Patients are typically normotensive. Rising serum urea
nitrogen and creatinine levels in a non-terminal patient may suggest nephropathy. For diagnosis
2
of HIVAN, total protein excretion should exceed 100 mg/m in a child or 200-500 mg in an
adult. The proteinuria can reach the nephrotic range. Albuminuria and lipiduria are typically
absent with HIVAN.[927,928]
Adults with HIVAN tend to progress rapidly to end stage renal disease and survival is
only a matter of months, with those persons having just HIV infection living longer than those
with clinical AIDS. In children, HIVAN has a less fulminant course. The use of antiretroviral
therapy slows the progression to renal failure.[929]
The kidneys with HIVAN can be grossly enlarged from 10 to 25%, appearing echogenic
by ultrasound. However, they are not atrophic, even in the later stages. The most common renal
biopsy finding, seen in over 80% of cases, is focal segmental glomerulosclerosis (FSGS).
Diffuse mesangial hypercellularity is the most common pattern seen in children. Other
histologic patterns that may be seen include membranoproliferative glomerulonephritis, minimal
change disease, and membranous glomerulonephritis. A variety of other patterns can occur
including proliferation of renal tubular and visceral epithelial cells (podocytes), tubular
microcystic formation, edema, interstitial fibrosis, and infiltration of the interstitium with
leukocytes. Over half of renal biopsies in HIVAN will demonstrate collapsed glomeruli, and this