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August 04, 2020
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Vitamin D does not appear to slow vascular calcification progression in CKD

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In the course of 18 months, supplementation with cholecalciferol did not attenuate vascular calcification progression in patients with chronic kidney disease and vitamin D insufficiency, though it did restore 25-hydroxyvitamin D levels.

According to Farid Samaan, MD, PhD, of Federal University of São Paulo in Brazil, and colleagues, hypovitaminosis D has shown associations with increased cardiovascular morbidity and mortality in both the general population and in patients CKD. The researchers noted that of these cardiovascular abnormalities, vascular calcification is of “major interest.”

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“As hypovitaminosis D is a frequent finding in patients with CKD, Kidney Disease Outcomes Quality Initiative (KDOQI) and Kidney Disease: Improving Global Outcomes (KDIGO) recommend to assess and restore 25(OH)D concentrations by vitamin D supplementation in this population,” they wrote. “Cholecalciferol, also known as vitamin D3, is a type of vitamin D frequently used in clinical practice. It has high affinity to hepatic 25-hydroxylase, vitamin D–binding protein, and vitamin D receptor.”

Contending that data related to the impact of vitamin D supplementation on vascular calcification in patients with CKD are “scarce and controversial,” Samaan and colleagues randomized 44 patients with CKD stages 3 to 4 and hypovitaminosis D to receive either cholecalciferol or placebo for 18 months. All patients had a creatinine clearance between 15 mL/min/1.73 m2 and 60 mL/min/1.73 m2 and serum 25(OH)D level less than 30 ng/mL, with 24 patients also being vitamin D deficient (defined as 25(OH)D level < 15 ng/mL). Researchers noted that patients with vitamin D deficiency were separately analyzed and all received cholecalciferol.

In the study period, researchers observed no changes in vascular calcification in patients with vitamin D insufficiency who were treated with cholecalciferol, though increases were seen in the placebo group. Further findings indicated renal function did not change for either group.

Regarding restoration of 25(OH)D levels, researchers found significant increases for patients with vitamin D insufficiency treated with either cholecalciferol or placebo, though the increases were greater for treated patients (86% of treated patients reached 25(OH)D 30 ng/mL at 18 months).

For patients with vitamin D deficiency, vascular calcification progressed (265 AU to 333 AU) and renal function declined (33 mL/min/1.73 m2 to 23 mL/min/1.73 m2), despite treatment with cholecalciferol. Treatment did, however, appear to restore 25(OH)D levels for these patients, with 83% achieving normal levels at 18 months.

“The long-term use of cholecalciferol, vitamin D in the nutritional form, is safe and effective in restoring 25(OH)D levels in pre-dialysis patients with CKD,” Samaan and colleagues wrote of the findings. “Nevertheless, vitamin D supplementation did not attenuate [vascular calcification] VC progression in CKD patients with hypovitaminosis D.”