Vitamin D deficiency aggravates ischemic acute kidney injury in rats

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 cyclin‐dependent kinase inhibitor and genomic target of 25‐hydroxyvitamin D, which is in...

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Published in:	Physiological reports Vol. 3; no. 3; pp. e12331 - n/a
Main Authors:	Bragança, Ana Carolina, Volpini, Rildo A., Canale, Daniele, Gonçalves, Janaína G., Shimizu, Maria Heloisa M., Sanches, Talita R., Seguro, Antonio C., Andrade, Lúcia
Format:	Journal Article
Language:	English
Published:	United States John Wiley & Sons, Inc 01-03-2015 BlackWell Publishing Ltd
Subjects:	25-Hydroxyvitamin D Acute kidney injury Aquaporin 2 Body weight Cell cycle Cell injury Cell proliferation Cyclin-dependent kinase inhibitor p21 Diet Enzyme inhibitors Excretion Glomerular filtration rate Ischemia Kidneys Kinases Nutrient deficiency Original Research Physiology Reperfusion Rodents Urine Vitamin D vitamin D deficiency Vitamin D receptors Vitamin deficiency cyclin‐dependent kinase inhibitor p21 Acute kidney injury vitamin D deficiency vitamin D receptors
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Summary:	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 cyclin‐dependent 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. VDD aggravates AKI. We speculate that the way in which 25(OH)D controls renal inflammation, proliferation and cell injury in ischemic AKI is by altering p21, and VDRs might constitute one of the pathways of that mechanism.
Bibliography:	Fundação de Amparo à Pesquisa do Estado de São Paulo Funding Information (FAPESP, São Paulo Research Foundation, Grant nos. 2010/52294‐0 and 2012/03025‐1, respectively). A C de Bragança is the recipient of a grant from the Brazilian Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES, Office for the Advancement of Higher Education); Drs Seguro and Andrade are recipients of grants from the Brazilian Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq, National Council for Scientific and Technological Development; Grant nos. 306148/2013‐7 and 302835/2009‐1, respectively). Drs Volpini and Sanches are recipients of grants from the ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Funding Information Drs Volpini and Sanches are recipients of grants from the Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP, São Paulo Research Foundation, Grant nos. 2010/52294-0 and 2012/03025-1, respectively). A C de Bragança is the recipient of a grant from the Brazilian Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES, Office for the Advancement of Higher Education); Drs Seguro and Andrade are recipients of grants from the Brazilian Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq, National Council for Scientific and Technological Development; Grant nos. 306148/2013-7 and 302835/2009-1, respectively).
ISSN:	2051-817X 2051-817X
DOI:	10.14814/phy2.12331