Background: Vitamin D deficiency is widely prevalent in chronic kidney disease [CKD] patients. The aim of our study was to determine whether losses of vitamin D binding protein [VDBP] in urine and dialysate contribute to circulating 25-hydroxyvitamin D [25OHD] levels in chronic peritoneal dialysis [PD] patients.
Methods: Dialysate, serum, and urine VDBP levels were measured in 16 children on PD and compared with serum and urine VDBP in ten CKD4-5 patients. Serum VDBP levels were correlated with total circulating 25OHD and peritoneal VDBP losses.
Results: The mean age of the study population was 9.4 ± 3.8 years and the median time on dialysis 7.5 (1-18) months. In CKD4-5 patients, urinary VDBP losses were >300-fold higher than seen in age-matched healthy children and correlated with urinary albumin loss (p = 0.0008). There was a significant correlation between serum VDBP and total dialysate and urine losses of VDBP (p = 0.03, r = -0.53). Dialysate VDBP losses correlate with dialysate albumin loss (p = 0.01). VDBP losses in the long daytime dwell were higher than in the overnight drain (p = 0.04). Serum VDBP levels were lower in children with a longer dialysis vintage (p = 0.0004, r = -0.77). In PD patients, the mean total loss of VDBP in dialysate and urine was 1.91 ± 1.6 μmol/day, equivalent to ~7% of the total circulating level of VDBP in healthy controls. There was no correlation between 25(OH)D and VDBP.
Conclusions: Peritoneal VDBP losses mirror both dialysate and urinary albumin losses, and are associated with a longer dialysis vintage but do not contribute to vitamin D deficiency in children on PD.
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http://dx.doi.org/10.1007/s00467-011-2045-0 | DOI Listing |
Pediatr Res
February 2019
Department of Biomedicine, Aarhus University, Aarhus, Denmark.
Background: Vitamin A and D deficiencies are common in preterm infants. Megalin is an endocytic receptor in the proximal tubule, which reabsorbs retinol-binding protein (RBP) and vitamin D-binding protein (VDBP). Although the proximal tubule is immature in preterm infants, little is known about megalin expression during kidney development.
View Article and Find Full Text PDFBiomed Res Int
March 2016
Institute 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.
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.
Pediatr Nephrol
April 2012
Renal Unit, Great Ormond Street Hospital for Children NHS, Trust and Institute of Child Health, London, United Kingdom.
Background: Vitamin D deficiency is widely prevalent in chronic kidney disease [CKD] patients. The aim of our study was to determine whether losses of vitamin D binding protein [VDBP] in urine and dialysate contribute to circulating 25-hydroxyvitamin D [25OHD] levels in chronic peritoneal dialysis [PD] patients.
Methods: Dialysate, serum, and urine VDBP levels were measured in 16 children on PD and compared with serum and urine VDBP in ten CKD4-5 patients.
Exp Diabetes Res
December 2011
Arkansas Children's Hospital Research Institute, Department of Pediatrics, University of Arkansas for Medical Sciences, 1 Children's Way, Slot 512-6, Little Rock, AR 72202, USA.
Microalbuminuria in humans with Type 1 diabetes (T1D) is associated with increased urinary excretion of megalin, as well as many megalin ligands, including vitamin-D-binding protein (VDBP). We examined the DBA/2J diabetic mouse, nephropathy prone model, to determine if megalin and VDBP excretion coincide with the development of diabetic nephropathy. Megalin, VDBP, and 25-hydroxy-vitamin D (25-OHD) were measured in urine, and genes involved in vitamin D metabolism were assessed in renal tissues from diabetic and control mice at 10, 15, and 18 weeks following the onset of diabetes.
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