ABNORMAL URINARY PROTEIN EXCRETION IN HIV-INFECTED PATIENTS

HIV infection has been associated with a variety of renal diseases, although the pathogenesis of such dysfunction is unknown. To determine whether HIV-infection associated with glomerular permeability defects, and if so, the prevalence of the finding, we studied patients with various stages of HIV infection. Urine samples from 505 outpatients with HIV infection (without hypertension, azotemia, or dipstick proteinuria), 41 normal controls and 40 febrile non-HIV positive, hospitalized patients with infectious diseases were analyzed for the urinary microalbumin/creatinine ratio (UmuA/Cr), a sensitive indicator of incipient renal disease in diabetes mellitus and hypertension, and the urinary beta2-microglobulin/creatinine ratio (Ubeta2/Cr), an indicator of renal tubular function. Microalbumin concentration was measured by ELISA. Beta2-microglobulin concentration was measured by an enzyme immunoassay. HIV-infected outpatients had higher mean UmuA/Cr than normal subjects, but not febrile hospitalized controls. The prevalence of an increased UmuA/Cr was 29.8% in the HIV-infected outpatient population. There was no difference in the ratio between Black and White HIV-infected outpatients, HIV-infected outpatients treated or untreated with zidovudine (AZT), or HIV infected outpatients untreated with any drug. There was no difference between UmuA/Cr in stage II, III or IV HIV-infected patients when assessed by analysis of variance. A similar pattern was noted with Ubeta2/Cr. The prevalence of an increased Ubeta2/Cr ratio was 37.7% in HIV-infected outpatients. Increased urinary albumin and beta2-microglobulin excretion, not associated with drug therapy, is present in patients with early HIV infection. This finding may be a nonspecific effect due to immune abnormalities, disordered cytokine production, or other factors, such as coexistent viral infections, consistent with ''febrile'' proteinuria. Alternatively, increased urinary protein excretion in HIV-infected patients may be an indication of the existence of intrinsic glomerular and tubular defects. The relationship of these abnormalities to the development of HIV nephropathy is uncertain and is an area for further investigation.