Vitamin D Binding Protein Is Not Involved in Vitamin D Deficiency in Patients with Chronic Kidney Disease.

Marta Kalousova,Tomas Zima,Sylvie Dusilova-Sulkova,Vladimir Tesar,Oskar Zakiyanov,Roman Safranek,Milada Kostirova

doi:10.1155/2015/492365

Abstract

Objective. This study was designed to evaluate vitamin D status with separate determination of 25-OH D2 and 25-OH D3 and its relationship to vitamin D binding protein (VDBP) in patients with chronic kidney disease (CKD) and long-term haemodialysis patients (HD). Methods. 45 CKD patients, 103 HD patients, and 25 controls (C) were included. Plasma vitamin D concentrations were determined using chromatography and VDBP in serum and urine in CKD using enzyme immunoassay. Results. Plasma vitamin D levels were lower in CKD (30.16 ± 16.74 ng/mL) and HD (18.85 ± 15.85 ng/mL) versus C (48.72 ± 18.35 ng/mL), P < 0.0001. 25-OH D3 was the dominant form of vitamin D. Serum VDBP was higher in CKD (273.2 ± 93.8 ug/mL) versus C (222 ± 87.6 ug/mL) and HD (213.8 ± 70.9 ug/mL), P = 0.0003. Vitamin D/VDBP ratio was the highest in C and the lowest in HD; however, there was no correlation between vitamin D and VDBP. Urinary concentration of VDBP in CKD (0.25 ± 0.13 ug/mL) correlated with proteinuria (r = 0.43, P = 0.003). Conclusions. Plasma levels of vitamin D are decreased in CKD patients and especially in HD patients. 25-OH D3 was the major form of vitamin D. Despite urinary losses of VDBP, CKD patients had higher serum VDBP concentrations, indicating compensatory enhanced production. Vitamin D binding protein is not involved in vitamin D deficiency.

Highlights

Vitamin D plays important physiological roles in maintaining calcium and phosphate homeostasis and in many other biological processes
Plasma vitamin D levels were lower in chronic kidney disease (CKD) (30.16 ± 16.74 ng/mL) and haemodialysis patients (HD) (18.85 ± 15.85 ng/mL) versus C (48.72 ± 18.35 ng/mL), P < 0.0001. 25-OH D3 was the dominant form of vitamin D
Plasma vitamin D levels were significantly lower in CKD (30.16 ± 16.74 ng/mL) and HD (18.85 ± 15.85 ng/mL) patients versus (48.72 ± 18.35 ng/mL) in controls, P < 0.0001 (Table 2)

Summary

Introduction

Vitamin D plays important physiological roles in maintaining calcium and phosphate homeostasis and in many other biological processes. Vitamin D may be produced endogenously in the skin (ultraviolet irradiation converting 7-dehydrocholesterol to cholecalciferol, i.e., vitamin D3) or obtained from food or supplements (mostly ergocalciferol, i.e., vitamin D2, and D3, e.g., from fish sources). Both ergocalciferol and cholecalciferol must be doublehydroxylated. The product of the first hydroxylation in the liver, 25-hydroxyvitamin D (calcidiol, 25-OH D), is the major circulating vitamin D metabolite. Calcidiol is converted by the second (1α) hydroxylation to calcitriol, that is, dihydroxylated active form of vitamin D (1, 25-OH D). For production of circulating calcitriol, renal 1α-hydroxylase is responsible, and several nonrenal tissues and cell lines express their own 1α-hydroxylase activity [1,2,3,4]. As the liver hydroxylation is neither regulated nor rate limited, 25-OH vitamin D well represents vitamin D status in the body. Serum 25-OH D levels > 75 nmol/L (30 ng/mL) indicate sufficient vitamin D stores [1, 4]

Methods

Results

Conclusion