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      Interstitial nephritis caused by HIV infection by itself: a case report

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          Abstract

          Interstitial nephritis is a common cause of renal dysfunction. It is primarily caused by drugs, infections, or autoimmune disorders. Patients with human immunodeficiency virus (HIV) infection can develop interstitial nephritis, although it typically occurs because of the aforementioned etiologies and not as a direct consequence of HIV infection. Interstitial lesions may occur in patients with HIV-associated nephropathy (HIVAN). However, interstitial nephritis without the glomerular injuries characteristic of HIVAN, and without the risk factors described earlier, is very rare. Here, we describe a rare case of interstitial nephritis that was likely caused directly by HIV infection and not by other etiologies.

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          Most cited references18

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          Nef harbors a major determinant of pathogenicity for an AIDS-like disease induced by HIV-1 in transgenic mice.

          Transgenic (Tg) mice expressing the complete coding sequences of HIV-1 in CD4+ T cells and in cells of the macrophage/dendritic lineages develop severe AIDS-like pathologies: failure to thrive/weight loss, diarrhea, wasting, premature death, thymus atrophy, loss of CD4+ T cells, interstitial pneumonitis, and tubulo-interstitial nephritis. The generation of Tg mice expressing selected HIV-1 gene(s) revealed that nef harbors a major disease determinant. The latency and progression (fast/slow) of the disease were strongly correlated with the levels of Tg expression. Nef-expressing Tg thymocytes were activated and alpha-CD3 hyperresponsive with respect to tyrosine phosphorylation of several substrates, including LAT and MAPK. The similarity of this mouse model to human AIDS, particularly pediatric AIDS, suggests that Nef may play a critical role in human AIDS, independently of its role in virus replication.
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            The spectrum of renal histologies seen in HIV with outcomes, prognostic indicators and clinical correlations.

            Two hundred and twenty-one HIV-positive renal biopsies were analysed from Groote Schuur Hospital to determine outcomes and prognostic indicators based on histology and clinical features. The histology findings were compared with patient demographics, clinical and renal parameters, mortality, CD4 count and date of commencing combined anti-retroviral therapy (cART). Follow-up was between 1 and 3.5 years. We found a spectrum of renal histologies in HIV-positive patients of which HIV-associated nephropathy (HIVAN) was the most common histology. cART reduced the mortality in those with any feature of HIVAN by 57% [adjusted hazard ratio (AHR) 0.43, 95% confidence interval (CI) 0.22-0.85]. Of those patients with HIVAN who died, 79% died of renal failure as registered on their death certificate. Proteinuria and microcysts were shown to be poor prognostic indicators (AHR 1.36: 1.09-1.70 and 2.04: 1.24-3.37). In patients with HIVAN alone followed for up to 2 years on cART, estimated glomerular filtration rate remained stable and there was a trend towards decreased proteinuria. cART improved survival in patients with isolated immune complex disease. As mortality is improved in patients with any feature of HIVAN or isolated immune complex disease, cART should be initiated once any of these histological features are established. We believe the spectrum of disease that constitutes HIVAN needs to be more specifically defined. The ultimate outcome may be determined by the histological subtype.
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              Collapsing glomerulopathy in HIV and non-HIV patients: a clinicopathological and follow-up study.

              Collapsing glomerulopathy in HIV and non-HIV patients: A clinicopathological and follow-up study. Collapsing glomerulopathy (CG) is a pattern of renal injury that is seen in association with HIV infection and that is increasingly recognized in non-HIV patients. A review of native kidney biopsies with CG that were diagnosed between 1979 and 1997 in 18 HIV and 42 non-HIV patients is provided. HIV and non-HIV patients with CG were similar in terms of age, sex ratio, serum creatinine, proteinuria, the extent of collapsing and sclerosing glomerular lesions, and interstitial damage. A slight female predominance was found in both groups. In contrast to non-HIV patients, the HIV group was characterized by a high prevalence of blacks (94 vs. 57%), frequent tubuloreticular inclusions (76 vs. 29%), and microcystic tubular changes (72 vs. 40%). In 13 non-HIV patients, CG was associated with a systemic lupus erythematosus (SLE)-like disease (5), hepatitis C virus (HCV) infection (3), HTLV-I infection, MCTD, acute monoblastic leukemia, multiple myeloma, and cerebral arteritis. Overall, the renal survival of human immunodeficiency virus (HIV) and non-HIV patients with CG was not significantly different. Cox regression revealed that HIV infection had an adverse effect on short-term renal survival, with other significant risk factors being extensive interstitial fibrosis, high serum creatinine, proteinuria, and a low percentage of glomeruli with collapse. The slope of reciprocal creatinine was best predicted by the degree of proteinuria. Serum creatinine correlated with the extent of interstitial fibrosis, the male gender, and the percentage of glomeruli with collapse. Proteinuria was best predicted by the extent of effacement of podocyte foot processes. CG shares many clinicopathological similarities in HIV and non-HIV patients. In some non-HIV patients, CG was associated with autoimmune diseases, lymphoproliferative disorders, and viral infections.
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                Author and article information

                Journal
                Int J Gen Med
                Int J Gen Med
                International Journal of General Medicine
                International Journal of General Medicine
                Dove Medical Press
                1178-7074
                2016
                01 September 2016
                : 9
                : 311-314
                Affiliations
                [1 ]Department of Infectious Diseases
                [2 ]Department of General Internal Medicine, Kobe City Medical Center General Hospital
                [3 ]Division of Infectious Diseases
                [4 ]Department of Diagnostic Pathology, Kobe University Hospital
                [5 ]Department of Pathology, Kobe City Medical Center General Hospital, Kobe, Hyogo, Japan
                Author notes
                Correspondence: Kentaro Iwata, Division of Infectious Diseases, Kobe University Hospital, Kusunokicho 7-5-2, Chuoku, Kobe, Hyogo 650-0017, Japan, Tel +81 78 382 6296, Fax +81 78 382 6298, Email kentaroiwata1969@ 123456gmail.com
                Article
                ijgm-9-311
                10.2147/IJGM.S115393
                5012837
                d3a29806-346c-4194-b60c-d61fa13b8a33
                © 2016 Doi et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Case Report

                Medicine
                human immunodeficiency virus,interstitial nephritis,hiv-associated nephropathy
                Medicine
                human immunodeficiency virus, interstitial nephritis, hiv-associated nephropathy

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