Sequential Changes of Vitamin D Level and Parathyroid Hormone After Kidney Transplantation

Vitamin D deficiency and infection risk in kidney transplant recipients: A single‐center cohort study

“…Various non‐mutually exclusive explanations may be offered, such as the progressive reduction in the intensity of immunosuppression—thus rendering less relevant the contributing role of vitamin D—or the lower number of infectious events beyond post‐transplant month 1, with the subsequent detrimental impact on the statistical power. Moreover, the present study confirms the beneficial effect derived from KT on the vitamin D status also reported by other authors, with a significant increase in serum 25(OH)D levels throughout the first year after transplantation. Nevertheless, the 12‐month prevalence of vitamin D deficiency was still as high as 28.8%‐60% (depending on criteria used), in keeping with a sustained disturbance of the parathyroid hormone‐fibroblast growth factor‐23 axis caused by baseline ESRD, impaired graft function and immunosuppressive therapy …”

Elevated parathyroid hormone one year after kidney transplantation is an independent risk factor for graft loss even without hypercalcemia

“…Secondary hyperparathyroidism is a frequent complication of chronic kidney disease (CKD) and increases the risk of mortality and various other complications [1]. Although successful kidney transplantation (KTx) can alleviate secondary hyperparathyroidism to some extent [2,3], hyperparathyroidism often persists and adversely affects clinical outcomes despite improved kidney function [2][3][4][5][6]. Elevated parathyroid hormone (PTH) levels promote bone resorption, calcium (Ca) reabsorption from the tubular tubes, and Ca absorption from the intestinal tract by increasing the production of 1,25-dihydroxycholecalciferol, often causing hypercalcemia [7].…”

The effect of cholecalciferol supplementation on allograft function in incident kidney transplant recipients: A randomized controlled study

“…Vitamin D deficiency (i.e., low 25‐hydroxyvitamin D [25(OH)D] level) is commonly observed in kidney transplant recipients (KTRs), particularly in the early phase postransplant, due to catabolic effect of glucocorticoid and/or sun‐avoidance behavior 1,2 . We previously reported that low 25(OH)D levels predicted a rapid decline in estimated GFR (eGFR) in patients with less than 10 years after transplantation 3 .…”

“…Vitamin D deficiency (i.e., low 25‐hydroxyvitamin D [25(OH)D] level) is commonly observed in kidney transplant recipients (KTRs), particularly in the early phase postransplant, due to catabolic effect of glucocorticoid and/or sun‐avoidance behavior. 1 , 2 We previously reported that low 25(OH)D levels predicted a rapid decline in estimated GFR (eGFR) in patients with less than 10 years after transplantation. 3 Bienaimé et al presented that low 25(OH)D levels at 3‐month posttransplant were associated with lower glomerular filtration rate (GFR) and progression of allograft interstitial fibrosis at 12‐month posttransplant.…”