Rapid Renal Failure in AIDS-Associated Focal Glomerulosclerosis

Langs, Charles; Gallo, Gloria; Schacht, Robert G.; Sidhu, Gurdip S.; Baldwin, David S.

doi:10.1001/archinte.1990.00390140041009

Cited by 53 publications

(19 citation statements)

References 9 publications

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“…Similarly to proteinuria, the prevalence of HIVAN seems to be linked to the characteristics of the group studied, especially considering the predominance of HAART. Studies during the 80s and at the beginning of the 90s illustrated a prevalence of HIVAN in the black population of around 10%, reaching 20% in certain reports [2,3,29,30]. Since 1996, with the introduction of HAART, this prevalence has gradually been reduced.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of persistent proteinuria in stable HIV/AIDS patients and its association with HIV nephropathy

Cavalcante¹,

Coelho²,

Lacerda³

2007

Braz J Infect Dis

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Human immunodeficiency virus (HIV)-related glomerular disease is a cause of end-stage renal disease, though there is no recent data from Brazil concerning this syndrome. Persistent proteinuria (PPt) is the main marker for glomerular disease, especially levels above 1.5 g. We examined the prevalence of and associated risk factors for PPt, along with the prevalence of HIV-associated nephropathy (HIVAN) among AIDS patients. We interviewed 411 patients who were attended at the HIV/AIDS section of the Clinical Hospital of the Federal University of Pernambuco (Brazil) from January through June 2004. PPt was defined as a positive urine dipstick exam on at least two occasions. The analyzed risk factors were: black race, a low CD4 lymphocyte count (<200 cells/mm 3 ), an HIV RNA level of >100,000 copies/mL and patients on highly-active antiretroviral therapy (HAART). The patients were classified according to urinary protein/creatinine ratio (Up/Uc) < 1.0, 1.0-3.0 and > 3.0. Patients with Up/Uc >3.0 were submitted to renal biopsy. Among the 411 HIV/AIDS patients, the mean age was 37 years, 70% were male, 37.5% were black, the mean CD4 count was 363 cells/mm 3 (± 95), the mean RNA HIV count was 44,475 copies/mL (± 40,369), and 92% were on HAART. The prevalence of PPt was 5.6% (95% CI = 3.6 to 8.3%), and it was significantly associated with a low CD4 lymphocyte count (p<0.048). HIVAN was found in just one patient, and two patients improved after HAART.

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Section: Discussionmentioning

confidence: 99%

Prevalence of persistent proteinuria in stable HIV/AIDS patients and its association with HIV nephropathy

Cavalcante¹,

Coelho²,

Lacerda³

2007

Braz J Infect Dis

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“…14], As initially described in black intravenous drug users, the histological finding in kidney biopsy specimens from patients with the nephrotic syn drome associated with HIV disease is focal and segmental glomerulosclerosis [1], Several investigators have shown that, unlike the slow deterioration of renal function typi cal of most diseases associated with the nephrotic syn drome, a large proportion of the patients with Hivan pro gress very rapidly to ESRD. leading to initiation of renal replacement therapy [3,5,6]. …”

Section: Discussionmentioning

confidence: 99%

Zidovudine Is Beneficial in Human Immunodeficiency Virus Associated Nephropathy

et al. 1995

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Human immunodeficiency virus associated nephropathy (Hivan) is a distinct renal disease described in patients infected with the human immunodeficiency virus (HIV). Hivan is characterized by a nephrotic syndrome, enlarged kidneys, a histologic finding of focal and segmental glomerulosclerosis, and a very rapid progression to end-stage renal disease (ESRD). No therapeutic intervention has been shown, in a prospective evaluation, to either alter the course of established Hivan or to influence the emergence of Hivan in HIV-infected patients. We conducted a prospective study on 23 consecutively selected patients seen between 1989 and 1992 who were infected with the HIV, 14 (61%) of whom had significant proteinuria ( > 2+). Percutaneous kidney biopsy was performed in 5 (36%) of the 14 subjects who had significant proteinuria, and histologic examination of the kidney tissue revealed focal and segmental glomerulosclerosis in all 5 cases. Of the 14 subjects with proteinuria, 8 (57%) also had azotemia (serum creatinine level > 1.3 mg/dl). Nine (39%) of 23 subjects admitted intravenous drug use, while 9 (39%) of 23 subjects have had an opportunistic infection before enrollment in the study. The known duration of HIV infection before initiation of zidovudine therapy was 10.3 ± (SD) 8 months. The mean CD4 count before zidovudine therapy was 195.9 ± 117 (range 21-654) cells/mm³. The mean dose of zidovudine administered was 543 ± 117 (range 400-800) mg daily for a period of 20.4 ± 11 (range 6-38) months. The clinical course of renal disease in the study subjects was compared to that of a control cohort of 28 HIV-infected patients with the nephrotic syndrome, presenting in ESRD for initiation of renal replacement therapy during the study period, who had never been treated with zidovudine or any other antiretroviral drug. Of 28 control patients, 14 (50%) admitted intravenous drug use; the known duration of HIV infection before onset of ESRD was 14.6 ± 8.6 months. These 28 control patients had been seen at an outpatient facility between 1989 and 1992 for anasarca and proteinuria without azotemia. The mean serum creatinine concentration of the 23 study subjects before zidovudine therapy was 1.2 ± 0.4 (range 0.8-2.1) mg/dl. By contrast, 8 (35%) of 23 subjects who stopped zidovudine due to noncompliance progressed to ESRD within a mean of 8 ± 2 (range 4-12) weeks, and each was begun on renal replacement therapy. Of these 8 patients, 2 died 10 and 12 weeks, respectively, after initiation of maintenance hemodialysis. These 8 patients had been on zidovudine therapy for a mean of 9 ± 3 months before discontinuing the drug. Reinstituted zidovudine therapy had no obvious effect on their renal function. None of the 15 zidovudine-compliant subjects developed ESRD or worsening azotemia. The mean serum creatinine concentration at the end of the study period was 0.93 ± 0.2 mg/dl. All patients initially free of proteinuria remained so. In the control patients, the interval from presentation with anasarca and proteinuria to onset of ES...

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“…HIVAN predominantly affects African-Americans and can occur at any stage of HIV-infection. It is characterized clinically by nephrotic-range proteinuria and rapid progression to end-stage renal disease (ESRD) over a period of a few months [10]. The pathologic characteristics of HIVAN are focal segmental glomerulosclerosis (FSGS) with collapse of the glomerular tuft, cystic dilatation of the tubules with proteinaceous casts and marked interstitial inflammatory infiltrate [11].…”

Section: Introductionmentioning

confidence: 99%

Is the Prevalence of HIV-Associated Nephropathy Decreasing?

et al. 1999

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Initial reports have suggested that approximately 10% of patients with HIV-infection develop HIV-associated nephropathy (HIVAN). It has also been predicted that by the end of the decade, HIVAN is likely to become a third leading cause of end-stage renal disease (ESRD) in African-Americans between the ages of 20–64 years. As the morbidity and mortality from HIV-infection has decreased in the last few years, it is possible that prevalence of HIVAN is also changing. We therefore screened HIV-1-infected patients followed in our hospital for HIVAN. A screening urinalysis was performed in 557 HIV-1-infected adult patients between March and May 1998. Of these, 252 were outpatients and 305 were Texas Department of Criminal Justice inmates (TDCJI). Demographic and laboratory data of these patients was obtained from the HIV patients’ database. Fifty percent of the patients were African-American, 36.6% were Caucasian and 12.7% were Hispanic. The mean age of patients was 37 ± 8 years. Seventy-nine percent of the patients were males and a history of intravenous drug abuse (IVDA) was present in 28%. Twenty-three percent of the patients were concomitantly infected with hepatitis C virus, 4.1% were positive for hepatitis B surface antigen, and rapid plasma reagin test for syphilis was positive in 9.1%. In 38 patients who had more than 100 mg/dl (2+) proteins on screening urinalysis, total urinary proteins were quantitated by collecting 24 h urine specimens. Fifteen of these patients had urinary proteins more than 1.5 g/day (12 patients >3.5 g/24 h and 3 patients >1.5 g/24 h). A renal biopsy was done in 14 of these patients and clinical diagnosis of HIVAN was made in one patient who refused biopsy. Renal biopsies revealed HIVAN [9], diabetic nephropathy [2], membranoproliferative glomerulonephritis [2], Fibrillary glomerulonephritis [1]. All 10 patients (5 TDCJI and 5 outpatients) with HIVAN were African-American. Two of these 10 patients had a history of IVDA and another two were concomitantly infected with hepatitis C virus. The plasma viral load (Pvl) and total CD4 count was not different in patients with or without HIVAN [(Pvl log 10.05 ± 1.39 vs. 9.9 ± 2.18 copies/ml, p = 0.78) (CD4: 187 ± 192 vs. 288 ± 249 cells/μl, p = 1.17) mean ± SD]. We conclude that in our HIV-infected population HIVAN exclusively affected African-Americans and the prevalence in them was 3.5%.

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Rapid Renal Failure in AIDS-Associated Focal Glomerulosclerosis

Cited by 53 publications

References 9 publications

Prevalence of persistent proteinuria in stable HIV/AIDS patients and its association with HIV nephropathy

Prevalence of persistent proteinuria in stable HIV/AIDS patients and its association with HIV nephropathy

Zidovudine Is Beneficial in Human Immunodeficiency Virus Associated Nephropathy

Is the Prevalence of HIV-Associated Nephropathy Decreasing?

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