



Types of Kidney Problems May Be Changing as HAART Era Matures



XVIII International AIDS Conference, July 1823, 2010, Vienna
Mark Mascolini
Paris clinicians found that rates of HIVassociated nephropathy (HIVAN) are waning as the HAART era matures [1], confirming other work [2]. But relative rates of another kidney problem, noncollapsing ("classical") focal and segmental glomerulosclerosis (FSGS), are on the rise. This is a singlecenter study, so results must be interpreted cautiously. But the findings suggest that HIV clinicians and nephrologists should keep a sharp eye for different types of kidney dysfunction in their patients as the epidemic evolves.
HIVAN research since triple therapy arrived indicates that HAART "can change the natural history of HIVAN, not only by preventing its development but also by halting its progression once developed" [2].
The study involved 101 consecutive HIVinfected people at Hopital Tenon in Paris who had renal biopsies and a diagnosis of glomerular disease from 1996 through 2007, spanning much of the HAART era. The investigators collected clinical and biological data by chart review, and a renal pathologist reexamined all biopsies. The researchers defined HIVAN as classical FSGS with tubulointerstitial inflammation, microcystic dilatation, and diffuse podocyte foot process effacement.
Among 88 biopsied HIVpositive patients with complete data available, median estimated glomerular filtration rate was 40 mL/min/1.72 m(2), CD4 count 217, and viral load 3071 copies. Sixtythree patients (72%) were taking antiretrovirals.
Throughout the study period, the four main types of glomerular lesions were HIVAN (30%), classical FSGS (26%), undetermined glomerulonephritis (9%), and mesangial proliferative glomerulonephritis (7%). The investigators then divided the 88 HIVinfected patients by the year in which they were biopsied: 27 (31%) in 19962000, 29 (33%) in 20012003, and 32 (36%) in 20042007. The three groups did not differ substantially in age or CD4 count. Among patients with FSGS (either HIVAN or classical FSGS), the proportion with HIVAN dropped significantly through the three periods: 75% in 19952000, 69% in 20012003, and 29% in 20042007, P = 0.011). The proportion with classical FSGS rose accordingly: from 25%, to 31%, to 71%.
The three study periods also differed in percentage of blacks (85.7%, 77.3%, and 53.8%, P = 0.04), proportion taking antiretrovirals (63.0%, 65.5%, and 84.4%, not significant at P = 0.13), median duration of HIV infection (48, 108, and 114 months, P = 0.04), and median estimated glomerular filtration rate (20, 27, and 55 ml/min/1.73 m(2), P = 0.05).
People with HIVAN differed from those with classical FSGS in proportion of African Americans (88% versus 68.4%, odds ratio [OR] 0.3, P = 0.11), time since HIV infection (median 42 versus 108 months, P = 0.03), CD4 count (median 74 versus 367, P < 0.01), proportion with a CD4 count under 200 (80.8% versus 23.8%, OR 0.07, P < 0.01), proportion on triple antiretroviral therapy (50% versus 91.3%, OR 0.1, P < 0.01), proportion with an undetectable viral load (20% versus 61.9%, OR 6.5, P = 0.01), and proportion with hepatitis C (8.7% versus 31.8%, OR 4.9, P = 0.06). The classical FSGS group also had a higher proportion of people with hypertension, abnormal lipids, and lipodystrophy, and they had a significantly higher estimated glomerular filtration rate (median 10 mL/min/1.73 m(2) with HIVAN versus 52 with classical FSGS, P < 0.01).
The investigators proposed a HIVAN scale with 3 points for African American background, 8 points for a CD4 count under 200, 20 points for estimated glomerular filtration rate under 30 mL/min/1.73 m(2), and 3 points for lack of antiretroviral therapy. A HIVAN scale score above 21 had a sensitivity of 92%, a specificity of 81%, a positive predictive value of 67%, and a negative predictive value of 96% in predicting HIVAN.
The researchers concluded that they were not seeing only a relative increase in classical FSGS because of declining HIVAN prevalence, but "a real switch of FSGS types over time." They proposed that a HIVAN scale score at or below 21 could justify kidney biopsy.
Reference
1. Flateau C, Lescure FX, Plaisier E, et al. Glomerular lesions in HIV1infected patients: evolution from 1996 to 2007, on 88 consecutive renal biopsies. XVIII International AIDS Conference. July 1823, 2010. Vienna. Abstract WEAB0302.
2. Atta MG. Diagnosis and natural history of HIVassociated nephropathy. Adv Chronic Kidney Dis. 2010;17:5258.






