The synthesis of 1α,25-dihydroxyvitamin D3 (Calcitriol) takes place mostly in the kidneys through the action
of 1α-hydroxylase (CYP27B1) which converts 25(OH)D into 1,25(OH)2D3. Renal production of calcitriol is stimulated by
PTH, low calcium and low phosphate and it is reduced by high phosphate and FGF23. Binding of 1α,25-dihydroxyvitamin
D3 to its receptor (VDR) causes gut absorption of calcium and phosphate, decrease in PTH synthesis, stimulation of
FGF23. At the bone level calcitriol suppresses pre-osteoblasts and activates mature osteoblasts. VDR is present in a large
variety of cells that do not have any direct role in the regulation of mineral metabolism. Calcitriol regulates immune and
inflammatory response, cell turnover, cell differentiation, Renin production, reduces proteinuria and others.
In patients with Chronic Kidney Disease (CKD) there is a decrease in calcitriol that is apparent at early stages of renal
disease; this is probably due to the elevation of FGF23 which is present since very early stage of CKD. In CKD stage, 3-4
moderate doses of calcitriol are effective to control secondary hyperparathyroidism and observational studies suggest that
calcitriol therapy increases survival and slows the progression of renal disease as long as phosphate and calcium levels are
controlled. Calcitriol (0.5 µg calcitriol twice per week) has been effective in decreasing proteinuria in patients with IgA
In dialysis patients, the administration of calcitriol reduces serum PTH levels but it is also known that high doses of
calcitriol are associated with hypercalcemia and worse control of hyperphosphatemia. In kidney transplant patients, the
administration of calcitriol, 0.5 µg/48h prevents bone mass loss during the first few months after transplantation.