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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The constellation of nephrotic proteinuria, FSGS, and rapid loss of renal function in a patient infected with HIV-1 has been sufficiently widespread and well documented to justify identification as a specific renal syndrome, HIV-associated nephropathy. The position paper of the National Kidney Foundation-National Institutes of Health task force estimated in 1990 that 10,000 to 15,000 persons will develop renal disease in association with AIDS [94]. Management of these patients is complex, and many will reach ESRD and require dialysis treatment, posing additional care problems. Greater understanding of the pathogenesis of the renal disease should lead to treatments which will forestall the development of HIVAN and possibly other forms of fibrotic renal disease. The ultimate eradication of AIDS will consign this renal syndrome to an interesting footnote in the history of nephrology. Since that time is still far in the future, nephrologists will continue to be faced with the need to diagnose and treat HIV-1-infected patients with renal involvement.
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PMID:Human immunodeficiency virus-associated glomerulosclerosis. 756 98

We report experience from London hospitals which further illustrates the heterogeneous nature of HIV-associated nephropathy (HIVAN). Nineteen HIV-positive patients underwent renal biopsy from 1992 to 1994. Fourteen were male, five female. Eleven were Afro-Caribbean, 7 Caucasian and 1 Asian. Eleven patients had classical HIVAN with proteinuria, rapidly progressive renal failure and features of focal and segmental glomerulosclerosis (FSGS) on renal biopsy, and three of these had associated tubulo-interstitial nephritis (TIN). One further patient had TIN and tubular changes suggestive of HIVAN but no glomeruli were present in the biopsy. Other biopsy findings were of focal proliferative glomerulonephritis and TIN (1 patient), pauci-immune crescentic glomerulonephritis and TIN (1 patient), membranous nephropathy (1 patient), membranoproliferative nephropathy (1 patient) and haemolytic uraemic syndrome (2 patients). Of 11 patients with FSGS, seven died with median survival of 8 months (range 23 days-46 months) and five are still alive after median follow-up of 18 months (range 10-22 months). Of patients with glomerular disease other than FSGS, five died, with median survival of 3 months (range 1-27 months) and two have survived (10 and 27 months, respectively). Thirteen patients had renal failure, 10 of whom had FSGS. In 10 cases renal failure was acute and in two was the presenting feature of HIV infection. Thirteen patients underwent renal replacement therapy. Four received haemodialysis, and all died within one month. Nine patients received CAPD. Two were able to discontinue dialysis. Of the remaining seven, five died with median survival of 8 months (range 1.3-40 months) and two are alive 1 and 10 months after beginning dialysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:HIV-associated renal disease in London hospitals. 758 76

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 (> or = 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 > or = 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.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Zidovudine is beneficial in human immunodeficiency virus associated nephropathy. 761 46

Human immunodeficiency virus-associated nephropathy (HI-VAN) is a common form of nephropathy present in HIV-infected individuals that clinically presents with proteinuria that is frequently in the nephrotic range, less often with hematuria, and with a course that may evolve to irreversible azotemia ultimately resulting in renal failure. Pediatric and adult HIV-positive patients both experience HIVAN morphologically after displaying focal segmental glomerulosclerosis, diffuse mesangial hyperplasia, microcystic tubular dilatation, interstitial inflammation, edema, and fibrosis. There is minimal information regarding the interstitial inflammatory cell infiltrate, despite the possibility that these cells may play an important role in the etiology of HIVAN. This study was designed to characterize and compare several morphological and immunopathological features of clearly established HIVAN, particularly the hematopoietic cell markers present on the interstitial inflammatory cells and the state of T-lymphocyte activation (ie, class II expression). Quantitative grading of HIVAN kidneys showed that CD4-positive and CD8-positive T cells comprised the major cell populations in the interstitium, often with CD4-positive T cells exceeding or being equivalent in number to CD8-positive T cells. B cells and macrophages were negligible components of the infiltrate. Human leukocyte antigen-DR class II molecules were found to be increased on the interstitial T cells as well as on all glomerular cells and endothelial cells. There was no significant relationship established between the immunophenotype of the interstitial inflammatory cells and other morphological, ultrastructural, immunofluorescent, or clinical features. These data imply that the inflammatory infiltrate in HIVAN is largely composed of activated T cells. At this point the role of these interstitial T cells in HIVAN is undetermined, although it can be speculated that they may be participating as antiviral or autoreactive immune effector cells imparting renal injury in this entity.
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PMID:Immunopathological characteristics of in situ T-cell subpopulations in human immunodeficiency virus-associated nephropathy. 770 20

Albumin excretion, Analysis of urinary proteins by polyacrylamide gel electrophoresis (PAGE), and clinical evaluation were performed in 90 HIV-infected patients to assess subclinical renal involvement in HIV infection. Thirteen percent of all patients showed an albumin excretion > 20 mg/liter. Seven of four homosexual patients had albuminuria. Albuminuria occurred exclusively with T4 cell counts below 200/mm3. Polyacrylamide gel electrophoresis indicated glomerular lesions and showed no tubular proteinuria in patients with increased albumin excretion. It is concluded that subclinical renal involvement is not uncommon in HIV infection with T4 cell counts > 200/mm3. HIV-associated nephropathy and heroin-associated nephropathy may not be the main causes of renal involvement. In some cases, opportunistic viral infections may be the cause of microalbuminuria.
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PMID:Albuminuria in HIV-infected patients. 791 29

Several renal pathologic entities have been reported to be associated with human immunodeficiency virus (HIV) infection. The most common is focal glomerulosclerosis, but several different types of glomerulonephritis have been observed in patients with HIV infection and the acquired immunodeficiency syndrome. The mechanisms involved in the pathogenesis of the kidney disease remain obscure. We studied an HIV-infected patient treated with interferon-alpha who had developed proteinuria and membranoproliferative glomerulonephritis to determine whether the renal disease was associated with HIV infection or with chemotherapy. Circulating HIV antibodies were assessed by enzyme-linked immunosorbent assay; circulating immune complexes (CICs) were measured by C'1q assay and isolated by polyethylene glycol precipitation, then subjected to gel electrophoresis and immunochemical analysis. Renal biopsy tissue underwent acid elution, and the eluates were analyzed similarly. In addition the eluted antibody and the antibody from the CIC were assessed by immunodiffusion with eluate and immune complex antigens. A single CIC was detected, which was composed of an immunoglobulin G antibody complexed to a 26-kd protein antigen that was shown to be interferon-alpha. Eluate from the renal biopsy tissue demonstrated identical material, which cross-reacted with the components of the isolated CIC. Immune complex renal diseases, such as membranoproliferative glomerulonephritis, may be related to biologic response modifying agents in patients with HIV infection. The relative roles of their biologic response modification and the disordered immunoregulation seen in such patients in the pathogenesis of the renal disease is unclear. Renal biopsy is necessary to assess the etiology of the renal disease in HIV-infected patients.
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PMID:Membranoproliferative glomerulonephritis in a patient treated with interferon-alpha for human immunodeficiency virus infection. 797 30

The case of a young, heterosexual man who was investigated for proteinuria is reported. A renal biopsy specimen showed a focal and segmental membranous glomerulopathy. He was later found to be HIV positive and died from cerebral infarction associated with HIV vasculitis 16 months after his initial presentation. Unusual forms of immune complex mediated glomerulopathies should alert the pathologist to the possibility of HIV associated disease.
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PMID:AIDS presenting as focal segmental membranous glomerulopathy. 813 37

A distinct form of renal disease has been described in patients at various stages of HIV infection that is becoming increasingly important as a cause of morbidity and mortality. Black race and intravenous drug abuse appear to predispose one to its development. The HIV-associated nephropathy is characterized by nephrotic-range proteinuria, rapid progression to end-stage renal disease, a diffuse sclerosing glomerulopathy with significant tubulo interstitial disease seen on light microscopy, and tubuloreticular inclusions seen via electron microscopy. The entity can be separated from heroin-associated nephropathy. The pathogenesis is unclear. Possibilities include direct invasion of the virus, effects of other viruses, genetic factors, immune factors, and multiple growth factors. Not all patients with HIV infection and renal disease have HIV-associated nephropathy. Because of prognostic and therapeutic implications, it is crucial to differentiate these lesions. Some reports suggest a possible beneficial effect of zidovudine therapy, but more study is required. Patient survival is dependent on the stage of HIV infection. Dialysis therapy does not appear to substantially prolong life in most patients with AIDS and irreversible renal failure. Therefore, a number of ethical issues have arisen that deal with medical futility.
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PMID:Human immunodeficiency virus-associated nephropathy: current concepts. 816 Jul 12

Analysis of pediatric AIDS surveillance revealed that 395 cases of pediatrics AIDS have been registered in Spain until the end of 1992. This accounts for about 3% of all cases of AIDS, a percentage higher than the cumulative pediatric percentage of 2% observed in USA and the rest of Europe. Although renal diseases is not considered a common clinical manifestation of AIDS, approximately 10% of the adults and 7% of pediatric AIDS patients are affected. To assess the situation of childhood HIV-associated nephropathy (HIVAN) in Spain, a survey of Spanish divisions of Pediatric Nephrology was undertaken in 1990. Three children with renal disease were identified. To know the actual prevalence of renal disease in HIV-infected children two years later, a new survey to 15 Spanish hospitals with divisions in Pediatric Nephrology was performed. The questionnaire included a retrospective analysis of their experience with HIV infected children and renal manifestations. The fourteen centers (93%) that responded to the questionnaire controlled 694 HIV-infected children (Class P-O: 454, Class P-1: 98, Class P-2: 142). Ten of them had screening program to detect renal disease in HIV infected children since 1989. Only two centers reported two new cases, one each, with clinical manifestations of HIV infection and renal disease, but without histologic confirmation one of them. They were two white girls, 24 and 2 months old respectively with proteinuria but without hematuria, chronic renal failure neither hypertension. Both patients died from infectious cause eleven months after and at the time of diagnosis respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[HIV-related nephropathy in children: the situation in Spain]. 816 1

A strain of mouse transgenic for the env gene of the HIV-1 virus was used to study the immunogenicity of a gp160-derived vaccine (the protein encoded by the HIV env gene) and its effect on disease progression. Untreated transgenic mice frequently developed a rapidly progressive renal disease similar to that affecting approximately 10% of HIV-infected humans. When transgenic mice were immunized with recombinant purified gp160, their edema, proteinuria, and serum BUN levels were substantially reduced and their survival prolonged (p < 0.01). The increased longevity of immunized transgenic mice correlated with the production of IgG antibodies reactive with gp160.
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PMID:Immunization with recombinant gp160 prolongs the survival of HIV-1 transgenic mice. 828 Apr 80


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