Vitamin D Effects on Bone Homeostasis and Cardiovascular System in Patients with Chronic Kidney Disease and Renal Transplant Recipients

Abstract

Poor vitamin D status is common in patients with impaired renal function and represents one main component of the complex scenario of chronic kidney disease–mineral and bone disorder (CKD–MBD). Therapeutic and dietary efforts to limit the consequences of uremia-associated vitamin D deficiency are a current hot topic for researchers and clinicians in the nephrology area. Evidence indicates that the low levels of vitamin D in patients with CKD stage above 4 (GFR < 15 mL/min) have a multifactorial origin, mainly related to uremic malnutrition, namely impaired gastrointestinal absorption, dietary restrictions (low-protein and low-phosphate diets), and proteinuria. This condition is further worsened by the compromised response of CKD patients to high-dose cholecalciferol supplementation due to the defective activation of renal hydroxylation of vitamin D. Currently, the literature lacks large and interventional studies on the so-called non-calcemic activities of vitamin D and, above all, the modulation of renal and cardiovascular functions and immune response. Here, we review the current state of the art of the benefits of supplementation with native vitamin D in various clinical settings of nephrological interest: CKD, dialysis, and renal transplant, with a special focus on the effects on bone homeostasis and cardiovascular outcomes.

Modulation of cardiometabolic risk and CardioRenal syndrome by oral vitamin D3supplementation in Black and White Southern Sahara residents with chronic kidney disease Stage 3: focus on racial and ethnic disparities

“…Regarding vitamin D supplementation, some authors have tested several doses as therapeutic targets to limit the CKD progression to dialysis stage [ 43 ]. It is important to note that currently no international consensus has been established on the optimal dose and vitamin D duration treatment in CKD [ 44 ]. Several doses and duration (higher versus lower; long versus short) of 25OHD-S to be used in the American black versus American white population to study the vitamin D metabolic effects [ 45 ].…”

Vitamin D and the Kidney: Two Players, One Console

“…Moreover, the 1α-hydroxylation of 25(OH)D is impaired due to damaged kidney tissue. The resulting hypocalcemia and hyperphosphoremia, secondary to kidney failure, lead to secondary hyperparathyroidism and increased serum levels of the hyperphosphaturic, osteocyte-derived fibroblast growth factor 23 (FGF23) [ 18 ]. PTH and FGF23 have opposite effects on the regulation of 1α-hydroxylase: while PTH enhances its expression in order to invert the trend of calcium loss, FGF23, which is triggered by phosphate retention, inhibits renal 1α-hydroxylase expression [ 7 ].…”

Key mechanisms of the relationship between vitamin D and cardiovascular disease

“…Поэтому его дефицит приводит к нарушениям минерального состава костной ткани и развитию вторичного гиперпаратиреоза, вследствие снижения уровня в паращитовидной железе VDR и кальцийчувствительных рецепторов с последующим снижением ингибирующих стимулов секреции ПТГ и чувствительности паращитовидной железы к ионизированному кальцию. Однако другие внепочечные клетки, такие как остеобласты, остеокласты и паращитовидные клетки, также могут синтезировать кальцитриол благодаря своей способности экспрессировать мегалин, кубилин и CYP27B [33].…”