Peer-reviewed veterinary case report
Vitamin D supplement effects on kidney disease hormones in dogs
By Miller, Matthew et al.·Published in Journal of veterinary internal medicine·2022·SAGE Veterinary Centers·View original on PubMed →
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Original publication title: Effect of calcifediol supplementation on renin-angiotensin-aldosterone system mediators in dogs with chronic kidney disease.
- Species:
- dog
Plain-English summary
A group of six adult dogs with chronic kidney disease (CKD) received calcifediol, a form of vitamin D, to see if it could help manage their condition. After three months of treatment, the dogs showed significantly higher levels of vitamin D in their blood, and a decrease in a specific enzyme related to kidney function. While the study was small, the results suggest that vitamin D supplementation might help lower certain harmful substances in dogs with CKD. If your dog has kidney issues, talk to your vet about whether vitamin D supplementation could be beneficial.
People also search for: dog chronic kidney disease treatment · vitamin D for dogs with kidney disease · calcifediol for dogs
Abstract
BACKGROUND: Chronic kidney disease (CKD) leads to low serum concentrations of vitamin D metabolites. Thus, hypovitaminosis D associated with CKD might contribute to disease progression via increased concentration of renin angiotensin aldosterone system (RAAS) mediators. OBJECTIVES: To evaluate whether supplementation with calcifediol affects equilibrium concentrations of selected mediators of the RAAS. We hypothesized that vitamin D supplementation will decrease concentration of circulating RAAS mediators in dogs with CKD. ANIMALS: Six client-owned adult dogs with IRIS Stage 2 and 3 CKD. METHODS: Prospective study. Serum 25-hydroxyvitamin D (25[OH]D), 1,25-dihydroxyvitamin D (1,25[OH]D), 24,25-dihydroxyvitamin D (24,25[OH]D), RAAS mediators (angiotensin I/II/III/IV/1-5/1-7, and aldosterone), and surrogate angiotensin converting enzyme (ACE) activity (calculated by the ratio of angiotensin II to angiotensin I) were evaluated at baseline, after 3 months of calcifediol supplementation, and 2 months after discontinuing administration of supplement. RESULTS: All serum vitamin D metabolite concentrations increased significantly by month 3 (P < .001): 25(OH)D (median 250 ng/mL; range, 204-310), compared to baseline (median 43.2 ng/mL; range, 33.8-58.3 ng/mL); 1,25(OH)D (median 66.1 pg/mL; range, 57.3-88.1 pg/mL) compared to baseline (median 35.2 pg/mL; range, 29.3-56.7 pg/mL); 24,25(OH)D (median 68.4 ng/mL; range, 22.1-142.0 ng/mL) compared to baseline (median 14.4 ng/mL; range, 9.0-21.3 ng/mL). Calculated ACE activity was significantly lower at month 3 (median 0.5; range, 0.4-1.0) compared to baseline (median 0.7; range, 0.6-1.3; P = .01). There were no significant differences in any of the evaluated RAAS variables at any other time-point. CONCLUSIONS AND CLINICAL IMPORTANCE: Short-term calcifediol supplementation in this small group of CKD dogs appeared to decrease ACE activity.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/35962709/