NDT Advance Access originally published online on November 26, 2007
Nephrology Dialysis Transplantation 2008 23(4):1457-1458; doi:10.1093/ndt/gfm692
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Reply
E-mail: yamakazu{at}xqb.biglobe.ne.jpSir,
We thank Dr Shahapuni for his comments on our recent paper [1]. As he describes, the ideal calcium (Ca) level of dialysate should be isocalcaemic to maintain a neutral calcium balance during dialysis. Theoretically, it may be desirable to determine the Ca level of dialysate in the individual patient, who receives various phosphate binders, vitamin D derivatives and so on, in accordance with each pre-HD Ca level. However, in routine clinical practice, it is too difficult to perform every HD treatment, while changing the contents of dialysate for each patient. We administered oral phosphate binders and vitamin D analogues [1 
-hydroxyvitamin D3 (alfacalcidol), 22-oxa-1, 25-dihydroxyvitamin D3 (22-oxacalcitriol)] to achieve the target serum levels of Ca, P and intact PTH just before HD: from 8.5 to 9.5 mg/dl for Ca; <6 mg/dl for P; from 100 to 300 pg/ml for intact PTH. In our patients, the mean value of pre-HD Ca was 8.99 ± 0.57 mg/dl under every HD treatment with a dialysate containing 3.0 mEq/l of calcium. Therefore, excess calcium transfer may have occurred after HD treatment, because the post-HD Ca level was higher than pre-HD Ca in all patients except three. These higher levels may be one of the risk factors for development of vascular calcification. However, it remains unknown whether a dialysate Ca concentration of 2.5 mEq/l, recommended by the K/DOQI guideline [2], would be adequate for most HD patients including ours, to prevent vascular calcification and the occurrence of secondary hyperparathyroidism.
As Dr Shahapuni points out, a negative correlation was found between 
Ca and vitamin D treatment (each number of patients was: no, 32; oral, 32; intravenous, 7) in our study. Ca was not significantly different in these three groups, but tended to be lower depending on the vitamin D dose (0.72 ± 0.0.38 mg/dl verses 0.63 ± 0.39 verses 0.25 ± 0.57 mg/dl). The serum pre-HD Ca levels significantly differed in the three groups (8.92 ± 0.54 mg/dl verses 8.92 ± 0.53 verses 9.63 ± 0.53 mg/dl, Friedman test; p = 0.0281). Therefore, higher pre-HD Ca concentration in the groups with intravenous vitamin D treatment may be correlated to a lower 
Ca. However, we have no evidence nor answer to his idea that vitamin D analogues may have a preventative effect on the increase of Ca. We furthermore have no comments on the difference degree of vascular calcification between the use of activated vitamin D derivatives, cholecalciferol or 25-OH vitamin D, because no patients were prescribed cholecalciferol and the 25-hydroxyvitamin D levels were not measured. To our knowledge, there are no reports that vitamin D itself directly improves or promotes vascular calcification in HD patients.
Ideal pre-HD Ca levels seem to be invalid (because serum Ca concentration tend to decline with higher serum P concentration) compared to P and Ca–P product. High levels of these parameters are well known to be associated with higher rate of vascular calcification, cardiovasucular events and death [3–5]. However, hypercalcemia is well known as one of the risk factors for vascular calcification, and several studies [6–8] have shown that the dose of calcium-based phosphate binders is associated with vascular calcification. At present, as Ix et al. describes [9], we should aim to control Ca, P and PTH within the target levels using adequate dose of oral phosphate binders and activated vitamin D derivates, in accordance with K/DOQI and Japanese guidelines [2,10], based on available scientific evidences. More studies on dialysate level, Ca/P metabolism, PTH and other hormones are needed to prevent vascular calcification in dialysis patients.
Conflict of interest statement. None declared.
First Department of Internal Medicine, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan
References
- Yamada K, Fujimoto S, Nishiura R, et al. Risk factors of progression of abdominal aortic calcification in patients on chronic haemodialysis. Nephrol Dial Transplant (2007) 22:2032–2037.
[Abstract/Free Full Text] - National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis (2003) 42:S1–S201.[Medline]
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[Abstract/Free Full Text] - Block GA, Klassen PS, Lazarus JM, et al. Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. J Am Soc Nephrol (2004) 15:2208–2218.
[Abstract/Free Full Text] - Guérin AP, London GM, Marchais SJ, et al. Arterial stiffening and vascular calcifications in end-stage renal disease. Nephrol Dial Transplant (2000) 15:1014–1021.
[Abstract/Free Full Text] - Goodman WG, Goldin J, Kuizon BD, et al. Coronary–artery calcification in young adults with end-stage renal disease who are undergoing dialysis. N Engl J Med (2000) 342:1478–1483.
[Abstract/Free Full Text] - Chertow GM, Burke SK, Raggi P, et al. Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients. Kidney Int (2002) 62:245–252.[CrossRef][Web of Science][Medline]
- Ix JH, Quarles LD, Chertow GM. Guidelines for disorders of mineral metabolism and secondary hyperparathyroidism should not yet be modified. Nat Clin Pract Nephrol (2006) 2:337–339.[CrossRef][Web of Science][Medline]
- Japanese Society for Dialysis Therapy. Guidelines for the management of secondary hyperparathyroidism in chronic dialysis patients. J Jpn Soc Dial Ther (2006) 39:1435–1456. (in Japanese).
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