Vitamin D deficiency is a potential risk factor for contrast-induced nephropathy

Author(s)

Luchi, Weverton M. ^{[1, 2]} ; Shimizu, Maria Heloisa M. ^[1] ; Canale, Daniele ^[1] ; Gois, Pedro Henrique F. ^[1] ; de Braganca, Ana Carolina ^[1] ; Volpini, Rildo A. ^[1] ; Girardi, Adriana C. C. ^[3] ; Seguro, Antonio C. ^[1]

Affiliation

^[1] Univ Sao Paulo, Sch Med, Div Nephrol, Med Invest Lab 12, BR-01246903 Sao Paulo - Brazil

^[2] Univ Fed Espirito Santo, Div Nephrol, Vitoria - Brazil

^[3] Univ Sao Paulo, Sch Med, Inst Heart, Lab Genet & Mol Cardiol, BR-01246903 Sao Paulo - Brazil

• Document type: Journal article
• Source: AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY; v. 309, n. 3, p. R215-R222, AUG 1 2015.
• Web of Science Citations: 10

Abstract

Vitamin D deficiency (VDD) is widespread in the general population. Iodinated (IC) or gadolinium-based contrast media (Gd) may decrease renal function in high-risk patients. This study tested the hypothesis that VDD is a predisposing factor for IC-or Gd-induced nephrotoxicity. To this end, male Wistar rats were fed standard (SD) or vitamin D-free diet for 30 days. IC (diatrizoate), Gd (gadoterate meglumine), or 0.9% saline was then administered intravenously and six groups were obtained as the following: SD plus 0.9% saline (Sham-SD), SD plus IC (SD + IC), SD plus Gd (SD + Gd), vitamin D-free diet for 30 days plus 0.9% saline (Sham-VDD30), vitamin D-free diet for 30 days plus IC (VDD30 + IC), and vitamin D-free diet for 30 days plus Gd (VDD30 + Gd). Renal hemodynamics, redox status, histological, and immunoblot analysis were evaluated 48 h after contrast media (CM) or vehicle infusion. VDD rats showed lower levels of total serum 25-hydroxyvitamin D {[}25(OH)D], similar plasma calcium and phosphorus concentration, and higher renal renin and angiotensinogen protein expression compared with rats fed SD. IC or Gd infusion did not affect inulin clearance-based estimated glomerular filtration rate (GFR) in rats fed SD but significantly decreased GFR in rats fed vitamin D-free diet. Both CM increased renal angiotensinogen, and the interaction between VDD and CM triggered lower renal endothelial nitric oxide synthase abundance and higher renal thiobarbituric acid reactive substances-to-glutathione ratio (an index of oxidative stress) on VDD30 + IC and VDD30 + Gd groups. Conversely, worsening of renal function was not accompanied by abnormalities on kidney structure. Additionally, rats on a VDD for 60 days displayed a greater fall in GFR after CM administration. Collectively, our findings suggest that VDD is a potential risk factor for IC-or Gd-induced nephrotoxicity most likely due to imbalance in intrarenal vasoactive substances and oxidative stress. (AU)

• FAPESP's process: 12/10146-0 - Molecular mechanisms of regulation of the proximal tubular function in hypertension
• Grantee: Adriana Castello Costa Girardi
• Support type: Regular Research Grants