Abstract

Objective: Elevated arterial stiffness has been described in hypertensive patients with CKD stage 3 and Vitamin D-deficiency in population-based cross-sectional studies. However, the role of supplementation in improving pulse wave velocity is controversial in most published series. Aim of this study is to analyze if the supplementation of VitD in never before treated hypertensive patients with CKD stage 3 and Vitamin D-deficiency modifies arterial stiffness. Design and method: Longitudinal study in the Hypertension Unit of a district hospital in 221 consecutive hypertensive patients with CKD stage 3 (CKD- EPI 30 – 60 ml/min), not treated before with VitD and with VitD-levels < 20 ng/ml. Arterial stiffness was measured as Pulse Wave Velocity (PWV, m/s) and Augmentation Index (%) in all the patients by brachial oscillometry (MOBIL-O-GRAPH®, IEM, Stolberg, Germany). Oral Calcifediol (266 mircrog/month) was prescribed to all the patients. A follow-up visit was performed after 12 months. Results: 126 (57%) patients were women, 95 men (43%). Mean age was 74.5 (SD ± 9.5), years, renal function measured by CKD-EPI was 49.3 ml/min (SD ± 7.2), BP averaged 130/66 mmHg, mean number of antihypertensive drugs was 3,5. Mean levels of baseline VitD were 15.6 ng/ml (SD ± 6.6), mean PWV was 11.0 m/s (SD ± 1.8). At follow-up after one year, mean levels of VitD in the whole group increased to 24.2 (DE ± 11.5), PWV was 11.1 m/s (DE ± 1.8). 63.8% of the patients were still under supplementation with VitD at follow-up while 36.2% had stopped the treatment. In the former, VitD increased to 29.0 ng/ml versus 15.3 ng/ml in the latter. Although the significant difference between those patients who kept the treatment and those who stopped were highly significant, no significant change of PWV was found between the two groups at follow-up. Conclusions: Correction of VitD-deficiency in hypertensive patients with CKD stage 3 and Vitamin D-deficiency is readily feasible, but in our study it did not translate into a significant change in vascular damage, measured as decrease of PWV, suggesting that the relationship between variables of arterial stiffness and VitD metabolism is not causal.

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