Abstract
Vitamin D and calcitriol deficiency and insufficiency are frequently observed in chronic kidney disease (CKD) and dialysis patients (90%). The main consequences are secondary hyperparathyroidism (SHPT), leading to bone mass reduction, fractures, and vascular calcification, and increased mortality rate. Native vitamin D supplementation increases the serum 25-hydroxyvitamin D (25-D) and 1,25-dihydroxyvitamin D (1,25-D) levels, decreases the serum parathyroid hormone (PTH) level, improves hypocalcaemia, and decreases proteinuria and left ventricular hypertrophy. Measurement of 25-D serum levels enables the identification of patients with 25-D insufficiency, even if biological targets are lacking, as well as the verification of vitamin D dosage efficiency. Prescription of calcitriol and analogues helps to increase the serum 1,25-D levels, to treat SHPT and hypocalcaemia, and perhaps to improve the survival rate. Routine serum 1,25-D sampling is not recommended, but it could be useful when treating SHPT with calcitriol and analogues. It would be interesting to undertake randomized control trials comparing native compounds and/or calcitriol or analogues in terms of the hard outcomes in both CKD and dialysis patients.
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