Objective: Left ventricular hypertrophy (LVH) is highly prevalent in chronic kidney disease (CKD) and a risk marker for cardiovascular mortality. It was hypothesized that vitamin D deficiency could play an important role in the pathogenesis of left ventricular hypertrophy and dysfunction in CKD. An open-labelled randomized study was performed comparing the effect of alfacalcidol versus no treatment in patients with CKD 4, secondary hyperparathyroidism and LVH. The primary endpoint was regression of LVH. Secondary endpoints were changes in left ventricular function.
Material and methods: Twenty-four patients were screened. Of these, 14 had LVH according to the criteria used. Six were randomized to alfacalcidol and seven to no treatment. The patient follow-up was 6 months. Left ventricular mass and function were measured by echocardiography.
Results: Parathyroid hormone decreased by 72% and -3% in the alfacalcidol-treated and non-treated groups, respectively (p < 0.05), while serum Ca(2+) increased by 9% and -1.6%, respectively (p < 0.05), and serum phosphate was unchanged. The left ventricular mass index was unchanged, whereas fractional shortening (20% vs 2%, p < 0.005) and Tei index (36% vs 12%, p < 0.05) increased significantly. Systolic and diastolic blood pressure was unchanged.
Conclusion: Short-term treatment with alfacalcidol did not induce regression of LVH; however, left ventricular function became hyperdynamic but less effective in patients with CKD. This could be problematic in the long term.