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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Vitamin D deficiency aggravates ischemic acute kidney injury in rats

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Author(s):
de Braganca, Ana Carolina ; Volpini, Rildo A. ; Canale, Daniele ; Goncalves, Janaina G. ; Shimizu, Maria Heloisa M. ; Sanches, Talita R. ; Seguro, Antonio C. ; Andrade, Lucia
Total Authors: 8
Document type: Journal article
Source: PHYSIOLOGICAL REPORTS; v. 3, n. 3 MAR 2015.
Web of Science Citations: 14
Abstract

Vitamin D deficiency (VDD) increases the risk of death in hospitalized patients. Renal ischemia/reperfusion injury (IRI) induces acute kidney injury (AKI), which activates cell cycle inhibitors, including p21, a cyclindependent kinase inhibitor and genomic target of 25-hydroxyvitamin D, which is in turn a potent immunomodulator with antiproliferative effects. In this study, we assess the impact of VDD in renal IRI. Wistar rats were divided into groups, each evaluated for 30 days: control (receiving a standard diet); VDD (receiving a vitamin D-free diet); IRI (receiving a standard diet and subjected to 45-min bilateral renal ischemia on day 28); and VDD + IRI (receiving a vitamin D-free diet and subjected to 45-min bilateral renal ischemia on day 28). At 48 h after IRI, animals were euthanized; blood, urine, and kidney tissue samples were collected. Compared with IRI rats, VDD + IRI rats showed a more severe decrease in glomerular filtration rate, greater urinary protein excretion, a higher kidney/body weight ratio and lower renal aquaporin 2 expression, as well as greater morphological damage, characterized by increased interstitial area and tubular necrosis. Our results suggest that the severity of tubular damage in IRI may be associated with downregulation of vitamin D receptors and p21. VDD increases renal inflammation, cell proliferation and cell injury in ischemic AKI. (AU)

FAPESP's process: 10/52294-0 - Assessing the role of vitamin D in the development of postischemic acute kidney injury
Grantee:Rildo Aparecido Volpini
Support Opportunities: Regular Research Grants
FAPESP's process: 12/03025-1 - Pathophysiological study of urinary transporters along the nephron in mice knockout for Klotho gene: The importance of klotho protein in tubular transport, in the acidification mechanisms and in the urinary dilution and concentration
Grantee:Talita Rojas Cunha Sanches
Support Opportunities: Scholarships in Brazil - Post-Doctoral