ArticleThe American journal of pathology2011
Adverse host factors exacerbate occult HIV-associated nephropathy.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- NEF-Induced HIV-Associated Nephropathy Through HCK/LYN Tyrosine Kinases.The American journal of pathology · 2023Article
- Hantavirus Induced Kidney Disease.Frontiers in medicine · 2021Review
- HIV Promotes NLRP3 Inflammasome Complex Activation in Murine HIV-Associated Nephropathy.The American journal of pathology · 2016Article
- Tubular cell phenotype in HIV-associated nephropathy: role of phospholipid lysophosphatidic acid.Experimental and molecular pathology · 2015Article
- AT1R blockade in adverse milieus: role of SMRT and corepressor complexes.American journal of physiology. Renal physiology · 2015Article
- Hyperglycemia enhances kidney cell injury in HIVAN through down-regulation of vitamin D receptors.Cellular signalling · 2015Article
- VIP in HIV Diarrhea: Finding Links for the "Slim Disease".Frontiers in physiology · 2015Article
- Modulation of renin angiotensin system predominantly alters sclerotic phenotype of glomeruli in HIVAN.Histology and histopathology · 2014Article
- Renin angiotensin system modulates mTOR pathway through AT2R in HIVAN.Experimental and molecular pathology · 2014Article
- HIV compromises integrity of the podocyte actin cytoskeleton through downregulation of the vitamin D receptor.American journal of physiology. Renal physiology · 2013Article
- Rapamycin-induced modulation of HIV gene transcription attenuates progression of HIVAN.Experimental and molecular pathology · 2013Article
- Inhibition of renin activity slows down the progression of HIV-associated nephropathy.American journal of physiology. Renal physiology · 2012Article
- HIV-induced kidney cell injury: role of ROS-induced downregulated vitamin D receptor.American journal of physiology. Renal physiology · 2012Article
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Authors and funding
10 authors.
Funding
Abstract
In the present study, we hypothesized that HIV-1-induced occult HIV-associated nephropathy (HIVAN) would become apparent in the presence of adverse host factors. To test our hypothesis, Vpr mice (which display doxycycline-dependent Vpr expression in podocytes) with two, three, and four copies of the angiotensinogen (Agt) gene (Vpr-Agt-2, Vpr-Agt-3, and Vpr-Agt-4) were administered doxycycline for 3 weeks (to develop clinically occult HIVAN) followed by doxycycline-free water during the next 3 weeks. Subsequently, renal biomarkers were measured, and kidneys were harvested for renal histology. Vpr-Agt-2 developed neither proteinuria nor elevated blood pressure, and displayed minimal glomerular and tubular lesions only, without any microcyst formation. Vpr-Agt-3 showed mild glomerular and tubular lesions and microcyst formation, whereas Vpr-Agt-4 showed moderate proteinuria, hypertension, glomerular sclerosis, tubular dilation, microcysts, and expression of epithelial mesenchymal transition markers. Vpr-Agt-4 not only displayed enhanced renal tissue expression of Agt, renin, and angiotensin-converting enzyme, but also had higher renal tissue concentrations of angiotensin II. Moreover, renal cells in Vpr-Agt-4 showed enhanced expression of transforming growth factor-β, connective tissue growth factor, and vascular endothelial growth factor. These findings indicate that adverse host factors, such as the activation of the renin-angiotensin system, promote the progression of occult HIVAN to apparent HIVAN.
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