NDT Advance Access originally published online on November 28, 2006
Nephrology Dialysis Transplantation 2007 22(3):957-958; doi:10.1093/ndt/gfl693
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Reply
Email: uwe.querfeld{at}charite.deSir,
The complex issue of therapy with vitamin D derivates in the treatment of secondary hyperparathyroidism is further complicated in the paediatric age group: children and adolescents with CKD require adequate substitution of vitamin D to cover the demands of a growing skeleton and to obtain an adequate peak bone mass [1]. Failure to provide adequate vitamin D supplements may result in muscular weakness, bone deformities and fractures during school age and adolescence, and in overt rickets, immobilization and neurodevelopmental delay in young children.
Supplementation of vitamin D3 i.e. cholecalciferol, is recommended in paediatric patients with CKD with low 25 OHD-levels and such recommendations are found in nephrology textbooks [2] as well as in recent European paediatric guidelines [3].
The finding of low 1,25 (OH)2D3 serum levels in children with a low GFR [4] and of healing of skeletal lesions and improved linear growth after administration of 1,25 (OH)2D3 in some studies [5] provides the rationale for 1,25 (OH)2D3 (calcitriol) therapy in most children with advanced stages of CKD.
Vitamin D3 (cholecalciferol) substitution was to our knowledge not only performed in the Berlin patients, but also in the Heidelberg patients (J. Oh, personal communication); however, for reasons unknown to us, the cumulative dose of prescribed cholecalciferol was not evaluated in the latter study. Thus, the possibility that differences in the frequency of calcification are due to differences in vitamin D3 (cholecalciferol) prescription cannot be ruled out, although firm evidence is lacking. As we have suggested in our study, differences in calcification prevalence might be rather due to a generally much less aggressive approach to the prescription of active vitamin D preparations (i.e. calcitriol) in the Berlin patients. However, we are aware that both studies were retrospective and therefore, other factors may have played a role.
We agree that supplementation of cholecalciferol remains an important cornerstone of therapy in CKD. The recent article by Ritter et al. [6] has provided a new explanation, on a molecular level, of how vitamin D supplementation might be effective in suppression of PTH synthesis in CKD. The NKF K/DOQI guidelines recommend measurement of 25-OHD concentrations in stage 3 and 4 CKD and subsequent vitamin D2 or D3 supplementation in patients with a level <30 ng/ml (guideline 7). Interestingly, a recent study found that over 75% of renal transplant patients had 25-OHD deficiency, defined by serum levels <40 nmol/l [7]. Therefore, 25-OHD deficiency may be quite common, not only in patients with CKD and on dialysis [8] but also in transplanted patients, and should be corrected. In the latter (retrospective) study, 25-OHD-levels were an independent predictor of PTH levels; however, these authors have calculated from their data that a 75 nml/l increase in 25-OHD would only result in a maximal reduction in PTH of 2.0 pmol/l. These data underscore the clinical significance of 25-OHD deficiency and indicate the need for controlled prospective studies to define efficacy of vitamin D3 supplementation in such individuals.
Conflict of interest statement. None declared.
1Charité Universitätsmedizin Berlin
Berlin
2Universitäts-Kinderklinik
Rostock, Germany
References
- Greer FR and Krebs NF. (2006) Optimizing bone health and calcium intakes of infants, children, and adolescents. Pediatrics 1172:578–585.
- Querfeld U. (2005) Chronic renal failure in children. In Davison AM, Cameron JS, Grünfeld J-P (Eds.), et al. Oxford Textbook of Clinical Nephrology.(Oxford University Press, Oxford) pp. 2141–2163.
- Klaus G, Watson A, Edefonti A, et al. (2006) Prevention and treatment of renal osteodystrophy in children on chronic renal failure: European guidelines. Pediatr Nephrol 21:151–159.[CrossRef][Web of Science][Medline]
- Chesney RW, Hamstra AJ, Phelps M, DeLuca HF. (1983) Vitamin D metabolites in renal insufficiency and other vitamin D disorders of children. Kidney Int Suppl 15:S63–S69.[Medline]
- Chan JC, Kodroff MB, Landwehr DM. (1981) Effects of 1,25-dihydroxyvitamin-D3 on renal function, mineral balance, and growth in children with severe chronic renal failure. Pediatrics 68:559–571.
[Abstract/Free Full Text] - Ritter CS, Armbrecht HJ, Slatopolsky E, Brown AJ. (2006) 25-Hydroxyvitamin D[3] suppresses PTH synthesis and secretion by bovine parathyroid cells. Kidney Int 70:654–659.[CrossRef][Web of Science][Medline]
- Boudville NC and Hodsman AB. (2006) Renal function and 25-hydroxyvitamin D concentrations predict parathyroid hormone levels in renal transplant patients. Nephrol Dial Transplant 21:2621–2624.
[Abstract/Free Full Text] - Gonzalez EA, Sachdeva A, Oliver DA, Martin KJ. (2004) Vitamin D insufficiency and deficiency in chronic kidney disease. A single center observational study. Am J Nephrol 24:503–510.[CrossRef][Web of Science][Medline]
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