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Aim: Vitamin D is being increasingly recognized as an important player in disease. Hypovitaminosis D is widespread in chronic kidney disease (CKD) populations around the world. The vitamin D status of Indian CKD patients is not known. Methods: Levels of 25(OH) vitamin D and parathyroid hormone (PTH) were measured in adult north Indian male patients with newly diagnosed stage IV–V CKD and matched control subjects drawn from the same population. A total of 100 (34 stage IV and 66 stage V) patients with CKD and 72 controls were studied. Results: Only 4% control and 1% of CKD subjects had normal (>30 ng/mL) vitamin D levels. Approximately 68% of control and 77% of the CKD population had vitamin D deficiency (<15 ng/ml) whereas the remaining 38% control and 22% CKD patients had insufficient (15–30 ng/mL) vitamin D levels. Levels were lower in CKD subjects compared to their family members, and the CKD patients were significantly more likely to have severe vitamin D deficiency (<5 ng/mL). A strong negative correlation was noted between vitamin D and PTH. No significant correlation was found between vitamin D levels and body mass index, bodyfat percentage, serum albumin or calcium levels. Conclusion: Vitamin D deficiency is highly prevalent in north Indians, and this is more pronounced in CKD subjects. There is a significant inverse correlation between the vitamin D and PTH levels. The clinical significance of this deficiency and the potential benefits to be derived from vitamin D supplementation in this population merits further studies. [ABSTRACT FROM AUTHOR]

Vitamin D deficiency is common and associated with mortality in chronic kidney disease (CKD) patients. Cardiovascular disease (CVD) is the commonest cause of mortality in CKD patients. In a randomized, double blind, placebo controlled trial, we have recently reported favorable effects of vitamin D supplementation on vascular & endothelial function and inflammatory biomarkers in vitamin D deficient patients with non-diabetic stage 3–4 CKD (J Am Soc Nephrol 28: 3100–3108, 2017). Subjects in the placebo group who had still not received vitamin D after completion of the trial received two oral doses 300,000 IU of oral cholecalciferol at 8 weeks interval followed by flow mediated dilatation (FMD), pulse wave velocity (PWV), circulating endothelial and inflammatory markers (E-Selectin, vWF, hsCRP and IL-6), 125 (OH) 2 D, iPTH and iFGF-23 assessment at 16 weeks. 31 subjects completed this phase of the study. Last values recorded in the preceding clinical trial were taken as baseline values. Serum 25(OH)D and 1,25(OH) 2 D increased and FMD significantly improved after cholecalciferol supplementation [mean change in FMD%: 5.8% (95% CI: 4.0–7.5%, p < 0.001]. Endothelium independent nitroglycerine mediated dilatation, PWV, iPTH, iFGF-23 and IL-6 also showed favorable changes. The data further cement the findings of beneficial effects of correction of vitamin D deficiency on vascular function. [ABSTRACT FROM AUTHOR]

Vitamin D deficiency, cardiovascular disease and abnormal bone mineral metabolism are common in chronic kidney disease (CKD). Abnormal bone mineral metabolism has been linked to vascular calcification in CKD. Sclerostin has emerged as an important messenger in cross talk between bone-vascular axis. We analyzed sclerostin in subjects who participated in the randomized, double blind, placebo controlled trial investigating the effect of cholecalciferol supplementation on vascular function in non­diabetic CKD stage G3-4 and vitamin D ≤ 20 ng/ml [CTRI/2013/05/003648]. Patients were randomized (1:1) to receive either two directly observed oral doses of 300,000 IU of cholecalciferol or matching placebo at baseline and 8 weeks. Of the 120 subjects enrolled, 58 in the cholecalciferol group and 59 in the placebo group completed the study. At baseline, serum levels of sclerostin were similar in both groups (cholecalciferol - median;190pg/ml, IQR;140–260 pg/ml and placebo - median;180 pg/ml, IQR; 140–240 pg/ml, p = 0.67). 16 weeks after cholecalciferol supplementation, there was no change in level of sclerostin (mean change;1.10 pg/ml, 95%CI; −27.34 to 29.34 pg/ml, p = 0.25). However, a significant decrease in sclerostin level was noted in the placebo group (mean change; −31.94 pg/ml, 95%CI; −54.76 to −9.13 pg/ml, p = 0.002). Change (Δ) in sclerostin level at 16 weeks correlated negatively with Δ eGFR (r = −0.20, p = 0.03) and positively with Δuric acid (r = 0.37, p < 0.001) but not with Δ25(OH) D (r = 0.06, p = 0.54), Δ iPTH (r = − 0.03, p = 0.78) ΔFGF23 (r = − 0.08, p = 0.38) and Δ125 (OH) 2 D (r = − 0.04, p = 0.65). In conclusion, high dose cholecalciferol supplementation did not change sclerostin levels in non-diabetic stage 3–4 CKD subjects. [ABSTRACT FROM AUTHOR]