NDT Advance Access originally published online on December 8, 2007
Nephrology Dialysis Transplantation 2008 23(3):1068-1069; doi:10.1093/ndt/gfm693
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Reply
E-mail: giorgio.coen{at}gmail.comSir,
We thank Drs Cozzolino and Brancaccio for their interest in our publication on PTH as a risk factor of coronary calcifications in uraemic HD patients. Some explanations for the apparent inconsistencies of our results with those published in the international literature have already been given in the article. For example, we expressed some reservations on London et al.'s much quoted publication [1] concerning the population cohort they studied. As discussed in our article, quite a number of patients in the London et al. paper had been previously parathyroidectomized; by definition, therefore, they had a past history of secondary hyperparathyroidism. As for the article by Hak et al. [2], I do not feel that their results are at odds with our results. Patients with increased postmenopausal osteoporosis are probably in a relatively increased bone resorption state compared to bone formation, a condition which, similarly to our cases with secondary hyperparathyroidism, may favour calcium phosphate deposition in extraskeletal tissues. Some of the experimental results of Price et al. [3,4] may favour increased bone resorption as a cause of the extraskeletal calcification process. The latter, according to these authors’ experimental results, can be suppressed or prevented by administration of bisphosphonates. As for the abstract presented at the ERA-EDTA 2007 Congress, by Asci et al. [5], I must conclude that the levels of PTH serum levels explored in their study were much lower than in our publication, therefore excluding the cases of severe secondary hyperparathyroidism. Our group with PTH levels >600 pg/ml and significantly higher calcification scores had an average value of intact PTH of 1186 ± 511 pg/ml, while in the Asci et al. study the high turnover group had a value of PTH 343 ± 341 pg/ml. Asci et al. did not explore really severe secondary hyperparathyroidism and for that reason we felt that our data cannot be compared to their study. In addition, in the abstract there is no information about vitamin D and calcium administration in the low turnover patients.
I could add, as stated in our article, that our results are more in line with epidemiological observations [6], suggesting that mortality is increased in patients with elevated PTH values, and considering that cardiovascular mortality is the main cause of death, the association of elevated PTH levels, and also serum calcium, with increased coronary calcifications is a reasonable result.
Conflict of interest statement. None declared.
References
- Price PA, Faus SA, Williamson MK. Bisphosphonates alendronate and ibandronate inhibit artery calcification at doses comparable to those that inhibit bone resorption. Arterioscl Thromb Vasc Biol (2001) 21:817–824.
[Abstract/Free Full Text] - Price PA, Roublick AM, Williamson MK. Artery calcification in uremic rats is increased by a low protein diet and prevented by treatment with ibandronate. Kidney Int (2006) 70:1577–1583.[CrossRef][Web of Science][Medline]
- Ganesh SK, Stack AG, Levin NW, et al. Association of elevated serum PO4, CaxPO4 product and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients. J Am Soc Nephrol (2006) 12:2131–2138.
- London GM, Marty C, Marchais SJ, et al. Arterial calcification and bone histomorphometry in end-stage renal disease. J Am Soc Nephrol (2004) 15:1943–1951.
[Abstract/Free Full Text] - Hak AE, Pols HAP, van Hemert Am, et al. Progression of aortic calcification is associated with metacarpal bone loss during menopause. Arterioscler Thromb Vasc Biol (2000) 20:1926–1931.
[Abstract/Free Full Text] - Asci G, Ozkahya M, Duman S, et al. The link between cardiovascular and bone disease in hemodialysis patients. Nephrol Dial Transplant (2007) 22 (Suppl 6) [Abstract SaO012], vi217.
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