NDT Advance Access originally published online on September 11, 2007
Nephrology Dialysis Transplantation 2007 22(11):3354; doi:10.1093/ndt/gfm605
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Optimal dialysate calcium and vascular calcification
Correspondence and offprint requests to: Email: joki{at}oha.toho-u.ac.jpSir,
Yamada et al. [1] report that the rate of progression of aortic calcification is related to the increase of serum calcium during the haemodialysis session (
Ca), using a stepwise multivariate regression analysis. The only other serum parameter that exhibited an association with the progression of aortic calcification was CRP. The authors hypothesized that the excess calcium transferred into patients on intermittent haemodialysis treatment when using a dialysate calcium concentration of 3.0 mEq/l was responsible for this association.
We would like to ask why the authors did not correct for post-dialysis haemoconcentration, when calculating Ca? They could have proceeded to this correction easily, since they measured serum albumin and presumably also blood haemoglobin, although this is not indicated in the article.
We respectfully question the hypothesis that the perdialytic Ca is the major culprit. An alternative hypothesis is that higher serum calcium levels simply reflect higher haemoconcentration at the end of the dialysis session, and that this in turn is the expression of a greater removal of sodium and water in patients with larger interdialytic body weight gain. Although the authors failed to observe a correlation between Ca and ultrafiltration rate in univariate analysis (Table 2), there was a correlation between these two parameters in step-wise multivariate regression analysis (Table 3). Our hypothesis is supported by the latter positive association and also by the negative association of Ca with the serum calcium concentration before the dialysis session.
We therefore believe, in disagreement with the 2003 K/DOQI guidelines [2], that the dialysate calcium concentration should generally not be lowered to <3.0 mEq/l, unless patients are receiving high doses of active vitamin D derivatives and/or calcium-containing phosphate binders. Low calcium concentrations in the dialysis fluid may be hazardous in chronic haemodialysis patients with cardiovascular disease, who are hypotension-prone [3] and in those who are receiving calcimimetics. The latter have the capacity to lower serum calcium [4] and to delay the progression of vascular calcification [5,6].
Conflict of interest statement. Dr Drueke reports having received consulting fees, speaker fees, and a research grant from both Amgen and Genzyme.
Inserm U845, Necker Hospital Paris France
References
- Yamada K, Fujimoto S, Nishiura R, et al. Risk factors of the progression of abdominal aortic calcification in patients on chronic haemodialysis. Nephrol Dial Transplant (2007) 22:2032–2037.
[Abstract/Free Full Text] - Massry SG, Coburn JW, for the work group members of the K/DOQI Practice Guidelines for Bone Metabolism & Disease in Chronic Kidney Disease. Am J Kidney Dis (2003) 42:S1–S201.[Medline]
- Locatelli F, Covic A, Chazot C, Leunissen K, Luno J, Yaqoob M. Optimal composition of the dialysate, with emphasis on its influence on blood pressure. Nephrol Dial Transplant (2004) 19:785–796.
[Abstract/Free Full Text] - Block GA, Martin KJ, de Francisco AL, et al. Cinacalcet for secondary hyperparathyroidism in patients receiving hemodialysis. N Engl J Med (2004) 350:1516–1525.
[Abstract/Free Full Text] - Ivanovski O, Phan O, Nikolov I, et al. The calcimimetic R-568 prevents progression of calcification and atherosclerosis in apolipoprotein E deficient (EKO) mice with chronic renal failure (CRF) and secondary hyperparathyroidism (HPT) (Abstract SA-PO543). JASN (2006) 17:690A.
- Lopez I, Aguilera-Tejero E, Mendoza FJ, et al. Calcimimetic R-568 decreases extraosseous calcifications in uremic rats treated with calcitriol. J Am Soc Nephrol (2006) 17:795–804.
[Abstract/Free Full Text]
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