Presentation, pathology, and outcome of HIV associated renal disease in a specialist centre for HIV/AIDS

Williams, D I; Williams, Debbie; Williams, IG; Unwin, Robert J.; Griffiths, M H; Miller, R F

doi:10.1136/sti.74.3.179

Cited by 52 publications

(30 citation statements)

References 25 publications

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“…Of the 4,218 patients reported by the U.S. Renal Data System for the period of 1997-2001, 90.2% were African American (1). This observation has been replicated in studies in Europe and Asia and is not explained by the mode of viral transmission (15)(16)(17)(18)(19)(20)(21). Moreover, relatives of index cases with HIVAN show an increased prevalence of ESRD from all causes, † † with only a small fraction of these additional cases attributable to HIV-1 (22).…”

mentioning

confidence: 49%

Mapping a locus for susceptibility to HIV-1-associated nephropathy to mouse chromosome 3

Gharavi

Ahmad

Wong

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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HIV-1-associated nephropathy (HIVAN) is a major complication of HIV-1 infection with distinct pathologic features. Introduction of the HIV-1 genome into mice results in a renal disease with all of the histologic and clinical hallmarks of HIVAN on the FVB͞N genetic background (TgFVB). We assessed the influence of genetic background on the development or progression of HIVAN by making F1 hybrids of TgFVB with five other inbred strains (CBA, DBA͞2, CAST͞Ei, C3H͞He, BALB͞c) and determining phenotypes relevant to renal failure among transgenic offspring (histology, blood urea nitrogen, proteinuria, serum albumin, and serum cholesterol). We found striking variation in phenotypes among F1s, ranging from severe renal disease to no renal disease whatsoever (P < 0.001 for ANOVA across all groups). To map genes responsible for this variation, we produced a backcross of TgFVB͞CAST F1 ؋ TgFVB. By genome-wide analysis of linkage in 185 heterozygous transgenic backcross mice, we identified a locus on chromosome 3A1-3, HIVAN1, that showed highly significant linkage to renal disease [logarithm of odds (lod) score 4.9 at D3Mit203, accounting for 15% of the variance in renal disease]. Other loci on chromosomes 11, 14, and 16 were suggestive of linkage to renal disease, and a locus on chromosome 9 influenced serum cholesterol but not nephropathy. Interestingly, HIVAN1 is syntenic to human chromosome 3q25-27, an interval showing suggestive evidence of linkage to various nephropathies. These findings demonstrate a strong genetic influence on HIVAN and demonstrate a major renal disease susceptibility locus on mouse chromosome 3A1-3.

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mentioning

confidence: 49%

Mapping a locus for susceptibility to HIV-1-associated nephropathy to mouse chromosome 3

Gharavi

Ahmad

Wong

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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“…More than 50% of episodes are attributed to infection. Most patients have pre-renal failure, often resulting in acute tubular necrosis from sepsis and fluid depletion because of vomiting, diarrhea and poor intake (Williams et al, 1998). There are little reliable data available on the causes and incidence of acute HIV-related kidney injury in Africa, but it is clear that a different pattern of presentation from the developed world is observed.…”

Section: Acute Kidney Injurymentioning

confidence: 91%

The Outcome of HIV-Positive Patients Admitted to Intensive Care Units with Acute Kidney Injury

Nel¹,

Moosa²

2012

Renal Failure - The Facts

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“…Several glomerulopathies have been observed in HIVpositive patients, such as IgA nephropathy, membranous glomerulonephritis, proliferative glomerulonephritis, minimal change disease, and particularly the collapsing variant of focal segmental glomerulosclerosis, which is an usual presentation of HIV-associated nephropathy [10][11][12][13][14].…”

Section: Discussionmentioning

confidence: 99%

Anti-glomerular basement membrane glomerulonephritis in an HIV positive patient: case report

Monteiro¹,

Caron²,

Balda³

et al. 2006

Braz J Infect Dis

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We report on a case of a patient with HIV infection, diagnosed 18 months prior to the development of an anti-glomerular basement membrane (anti-GBM) rapidly progressive glomerulonephritis; this is probably the first report of such an association. A 30-year-old white man presented with elevation of serum creatinine (1.3 -13.5 mg/dL within one month). At admission, the urinalysis showed proteinuria of 7.2 g/L and 8,000,000 erythrocytes/mL. Renal biopsy corresponded to a crescentic diffuse proliferative glomerulonephritis mediated by anti-GBM, and serum testing for anti-GBM antibodies was positive; antinuclear antibodies (ANA) and anti-neutrophilic cytoplasmic antibodies (ANCA) were also positive. The patient underwent hemodyalisis and was treated with plasmapheresis, cyclophosphamide and prednisone. The association described here is not casual, as crescentic glomerulonephritis is not common in HIV-positive patients, anti-GBM glomerulonephritis is rare and anti-GBM antibodies are frequently observed in HIV-positive subjects when compared to the overall population. Based on the current case and on the elevated frequency of the positivity for such antibodies in this group of patients, it is advisable to be aware of the eventual association between these two conditions and to promote an active search for anti-GBM antibodies and early diagnosis of eventual urinary abnormalities in HIV-positive subjects, considering the severity of anti-GBM glomerulonephritis.

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Presentation, pathology, and outcome of HIV associated renal disease in a specialist centre for HIV/AIDS

Cited by 52 publications

References 25 publications

Mapping a locus for susceptibility to HIV-1-associated nephropathy to mouse chromosome 3

Mapping a locus for susceptibility to HIV-1-associated nephropathy to mouse chromosome 3

The Outcome of HIV-Positive Patients Admitted to Intensive Care Units with Acute Kidney Injury

Anti-glomerular basement membrane glomerulonephritis in an HIV positive patient: case report

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