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Effect of alfacalcidol on cardiac function in patients with chronic kidney disease stage 4 and secondary
Per Ivarsen1, Johan Vestergaard Povlsen, Kent Lodberg Christensen
1Departments of Nephrology, Aarhus University Hospital, Aarhus, Denmark. pi@dadlnet.dk
Insights
Short-term alfacalcidol treatment in chronic kidney disease (CKD) patients did not reduce left ventricular hypertrophy (LVH). However, it improved left ventricular function, potentially leading to long-term issues.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Left ventricular hypertrophy (LVH) is common in chronic kidney disease (CKD) and predicts cardiovascular mortality.
- Vitamin D deficiency may contribute to LVH and dysfunction in CKD patients.
Purpose of the Study:
- To investigate the effect of alfacalcidol on LVH and left ventricular function in CKD patients.
- To assess if alfacalcidol can reverse LVH in CKD with secondary hyperparathyroidism.
Main Methods:
- An open-label, randomized study comparing alfacalcidol to no treatment.
- 14 CKD patients with LVH were randomized; 6 received alfacalcidol, 7 did not.
- Echocardiography assessed left ventricular mass and function over 6 months.
Main Results:
- Alfacalcidol significantly decreased parathyroid hormone and increased serum calcium.
- Left ventricular mass index remained unchanged.
- Fractional shortening and Tei index improved, indicating hyperdynamic but less effective function.
Conclusions:
- Short-term alfacalcidol did not regress LVH in CKD patients.
- Left ventricular function became hyperdynamic but less effective, posing potential long-term risks.
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.
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