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- Title
Vitamin D deficiency contributes to vascular damage in sustained ischemic acute kidney injury.
- Authors
Bragança, Ana C.; Volpini, Rildo A.; Mehrotra, Purvi; Andrade, Lúcia; Basile, David P.
- Abstract
Reductions in renal microvasculature density and increased lymphocyte activity may play critical roles in the progression of chronic kidney disease (CKD) following acute kidney injury (AKI) induced by ischemia/reperfusion injury (IRI). Vitamin D deficiency is associated with tubulointerstitial damage and fibrosis progression following IRI-AKI. We evaluated the effect of vitamin D deficiency in sustained IRI-AKI, hypothesizing that such deficiency contributes to the early reduction in renal capillary density or alters the lymphocyte response to IRI. Wistar rats were fed vitamin D-free or standard diets for 35 days. On day 28, rats were randomized into four groups: control, vitamin D deficient (VDD), bilateral IRI, and VDD+IRI. Indices of renal injury and recovery were evaluated for up to 7 days following the surgical procedures. VDD rats showed reduced capillary density (by cablin staining), even in the absence of renal I/R. In comparison with VDD and IRI rats, VDD+IRI rats manifested a significant exacerbation of capillary rarefaction as well as higher urinary volume, kidney weight/body weight ratio, tissue injury scores, fibroblast- specific protein-1, and alpha-smooth muscle actin. VDD+IRI rats also had higher numbers of infiltrating activated CD4+ and CD8+ cells staining for interferon gamma and interleukin-17, with a significant elevation in the Th17/ T-regulatory cell ratio. These data suggest that vitamin D deficiency impairs renal repair responses to I/R injury, exacerbates changes in renal capillary density, as well as promoting fibrosis and inflammation, which may contribute to the transition from AKI to CKD.
- Subjects
VITAMIN D deficiency; VASCULAR diseases; ACUTE kidney failure; DISEASE progression; ISCHEMIA; DISEASE risk factors
- Publication
Physiological Reports, 2016, Vol 4, Issue 13, p1
- ISSN
2051-817X
- Publication type
Article
- DOI
10.14814/phy2.12829