Journal
KIDNEY INTERNATIONAL
Volume 83, Issue 4, Pages 626-634Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/ki.2012.445
Keywords
diabetic nephropathy; glomerulopathy; HIV
Categories
Funding
- NIH/NIDDK [1R01DK078897-01, 2012CB517601, P01DK056492, 5K08DK082760, T32 DK07757-12, 1F32 DK094635-01]
Ask authors/readers for more resources
With the widespread use of combination antiretroviral agents, the incidence of HIV-associated nephropathy has decreased. Currently, HIV-infected patients live much longer and often suffer from comorbidities such as diabetes mellitus. Recent epidemiological studies suggest that concurrent HIV infection and diabetes mellitus may have a synergistic effect on the incidence of chronic kidney disease. To address this, we determined whether HIV-1 transgene expression accelerates diabetic kidney injury using a diabetic HIV-1 transgenic (Tg26) murine model. Diabetes was initially induced with low-dose streptozotocin in both Tg26 and wildtype mice on a C57BL/6 background, which is resistant to classic HIV-associated nephropathy. Although diabetic nephropathy is minimally observed on the C57BL/6 background, diabetic Tg26 mice exhibited a significant increase in glomerular injury compared with nondiabetic Tg26 mice and diabetic wild-type mice. Validation of microarray gene expression analysis from isolated glomeruli showed a significant upregulation of proinflammatory pathways in diabetic Tg26 mice. Thus, our study found that expression of HIV-1 genes aggravates diabetic kidney disease. Kidney International (2013) 83, 626-634; doi:10.1038/ki.2012.445; published online 16 January 2013
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available