Transgenic and Infectious Animal Models of HIV-Associated Nephropathy

Rosenstiel, Philip; Gharavi, Ali G.; D’Agati, Vivette D.; Klotman, Paul E.

doi:10.1681/asn.2008121230

Cited by 54 publications

(44 citation statements)

References 61 publications

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“…The importance of HIV RNA in the development of HIVICK has been suggested by the failure to generate this entity in experimental models. Contrary to HIVAN, in which many HIV-1 transgenic models exhibit the clinical and pathologic features of HIVAN, none of these animal models exhibit features of HIVICK (28,29). This observation suggests that viral replication or immune responses to viral proteins may be essential to trigger HIVICK (30).…”

Section: Discussionmentioning

confidence: 91%

Comparison of Risk Factors and Outcomes in HIV Immune Complex Kidney Disease and HIV-Associated Nephropathy

Foy

Estrella²,

Lucas³

et al. 2013

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives HIV-associated nephropathy (HIVAN) is well described, but the clinical features of a group of renal pathologies characterized by Ig or immune complex depositions referred to as HIV-associated immune complex kidney disease (HIVICK) have not been well established. The objective of this study is to assess risk factors for HIVICK compared with contemporaneous control participants.Design, setting, participants, & measurements A nested case-control study of 751 HIV-infected patients followed from January 1996 to June 2010 was conducted. Groups were compared using the chi-squared test or ranksum analysis. Conditional logistic regression was used to estimate odds ratios (ORs) for HIVICK. Incidences of overall ESRD and with/without combined antiretroviral therapy (cART) exposure were calculated.Results HIVICK patients were predominantly African American (92%). Compared with matched controls, patients with HIVICK were more likely to have HIV RNA .400 copies/ml (OR, 2.5; 95% confidence interval [95% CI], 1.2 to 5.2), diabetes (OR, 2.8; 95% CI, 1.1 to 6.8), and hypertension (OR, 2.3; 95% CI, 1.2 to 4.5). Compared with HIVAN, patients with HIVICK had more antiretroviral therapy exposure, lower HIV viral loads, and higher CD4 and estimated GFR. ESRD was less common in the HIVICK versus the HIVAN group (30% versus 82%; P,0.001), and the use of cART was not associated with ESRD in HIVICK patients (25% versus 26; P=0.39).Conclusions HIVICK was predominantly observed in African-American patients and associated with advanced HIV disease. ESRD incidence is lower in HIVICK patients compared with those with HIVAN. Unlike HIVAN, cART use was not associated with the incidence of ESRD in HIVICK.

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Section: Discussionmentioning

confidence: 91%

Comparison of Risk Factors and Outcomes in HIV Immune Complex Kidney Disease and HIV-Associated Nephropathy

Foy

Estrella²,

Lucas³

et al. 2013

Clinical Journal of the American Society of Nephrology

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“…Proteinuria was first observed at 24 days of age. Around 20% of these mice died between 2 and 6 months with increased proteinuria, elevated blood urea nitrogen, edema, ascites, and hypoalbuminemia [37,38]. Pathologically, the kidneys from uremic animals demonstrate collapsing lesions at a certain time point, diffuse segmental and global glomerulosclerosis, and microcystic tubular dilatation.…”

Section: Hiv-nephropathy Modelmentioning

confidence: 99%

Recent advances of animal model of focal segmental glomerulosclerosis

Yang

Dettmar

Kronbichler³

et al. 2018

Clin Exp Nephrol

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In the last decade, great advances have been made in understanding the genetic basis for focal segmental glomerulosclerosis (FSGS). Animal models using specific gene disruption of the slit diaphragm and cytoskeleton of the foot process mirror the etiology of the human disease. Many animal models have been developed to understand the complex pathophysiology of FSGS. Therefore, we need to know the usefulness and exact methodology of creating animal models. Here, we review classic animal models and newly developed genetic animal models. Classic animal models of FSGS involve direct podocyte injury and indirect podocyte injury due to adaptive responses. However, the phenotype depends on the animal background. Renal ablation and direct podocyte toxin (PAN, adriamycin) models are leading animal models for FSGS, which have some limitations depending on mice background. A second group of animal models were developed using combinations of genetic mutation and toxin, such as NEP25, diphtheria toxin, and Thy1.1 models, which specifically injure podocytes. A third group of animal models involves genetic engineering techniques targeting podocyte expression molecules, such as podocin, CD2-associated protein, and TRPC6 channels. More detailed information about podocytopathy and FSGS can be expected in the coming decade. Different animal models should be used to study FSGS depending on the specific aim and sometimes should be used in combination.

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“…Reciprocal transplantation studies between Tg26 and wild-type mouse focusing on podocyte-specific expression of HIV genes showed that viral gene expression within the kidney itself played an important pathologic role in the development of HIVAN (Rosenstiel et al, 2009a;Bruggeman et al, 1997). Subsequent studies confirmed that HIV has an ability to infect renal epithelial cells (Marras et al, 2002) and HIV nucleic acid was found in podocytes, parietal epithelial cells, tubular epithelial cells, T-cells and macrophages in human HIVAN renal biopsies Tanji et al, 2006).…”

Section: Role Of Hivmentioning

confidence: 99%