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

Marta Kalousova1, Sylvie Dusilova-Sulkova2, Oskar Zakiyanov3

  • 1Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, U Nemocnice 499/2, 128 01 Prague, Czech Republic.

Insights

Vitamin D levels are significantly lower in chronic kidney disease (CKD) and hemodialysis (HD) patients. Despite urinary vitamin D binding protein (VDBP) losses, higher serum VDBP in CKD suggests compensatory production, but VDBP is not linked to vitamin D deficiency.

Area of Science:

  • Nephrology
  • Endocrinology
  • Nutritional Science

Background:

  • Vitamin D deficiency is common in patients with chronic kidney disease (CKD).
  • The role of vitamin D binding protein (VDBP) in vitamin D status in CKD and hemodialysis (HD) patients requires further elucidation.
  • Separate determination of 25-hydroxyvitamin D2 (25-OH D2) and 25-hydroxyvitamin D3 (25-OH D3) is crucial for accurate assessment.

Purpose of the Study:

  • To evaluate vitamin D status, specifically 25-OH D2 and 25-OH D3 levels, in CKD and HD patients.
  • To investigate the relationship between vitamin D levels and VDBP in serum and urine of these patient groups.
  • To compare vitamin D and VDBP levels in CKD and HD patients with healthy controls.

Main Methods:

  • Cross-sectional study including 45 CKD patients, 103 HD patients, and 25 controls.
  • Plasma vitamin D concentrations (25-OH D2 and 25-OH D3) were measured using chromatography.
  • Serum and urinary VDBP levels in CKD patients were determined by enzyme immunoassay.

Main Results:

  • Plasma vitamin D levels were significantly lower in CKD (30.16 ± 16.74 ng/mL) and HD (18.85 ± 15.85 ng/mL) patients compared to controls (48.72 ± 18.35 ng/mL).
  • 25-OH D3 was identified as the predominant form of vitamin D.
  • Serum VDBP was elevated in CKD patients (273.2 ± 93.8 ug/mL) compared to controls (222 ± 87.6 ug/mL) and HD patients (213.8 ± 70.9 ug/mL).
  • A significant correlation was observed between urinary VDBP and proteinuria in CKD patients (r = 0.43, P = 0.003).

Conclusions:

  • Vitamin D deficiency is pronounced in CKD and particularly in HD patients.
  • Elevated serum VDBP in CKD patients, despite urinary losses, suggests a compensatory increase in VDBP production.
  • Vitamin D binding protein levels do not appear to be directly involved in the pathogenesis of vitamin D deficiency in these patient populations.
Abstract

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