NDT Advance Access originally published online on November 28, 2007
Nephrology Dialysis Transplantation 2008 23(3):1067-1068; doi:10.1093/ndt/gfm687
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Is PTH a risk factor for cardiovascular calcifications in haemodialysis?
E-mail: mariocozzolino{at}hotmail.comSir,
We read with interest the article in NDT by Coen et al. [1], on the association between serum intact parathyroid hormone (iPTH) levels higher than 600 pg/ml and the severity of coronary calcifications in haemodialysis (HD) patients. In their manuscript, the authors divided 197 HD patients into four groups of serum iPTH levels: (A) 0–150 pg/ml; (B) 150–300 pg/ml; (C) 300–600 pg/ml; (D) >600 pg/ml. Surprisingly, a higher coronary calcification score was not associated with lower serum iPTH levels, but only HD patients with evidence of secondary hyperparathyroidism (SHPT) show significant increases in arterial calcium deposition (group D). To our knowledge, this is the first observation in which the association between severe SHPT and cardio-vascular calcification is clearly documented. Nonetheless, we would like to raise a point of discussion, because other studies have shown different results.
In normal renal function postmenopausal women, atherosclerosis and osteoporosis are major causes of morbidity and mortality, and a graded inverse cross-sectional association between the extent of aortic calcification and metacarpal bone mass and density was found [2]. Furthermore, London et al. [3] studied the bone histomorphometry and arterial calcification (AC) score in 58 HD patients. In contrast to the results of this letter, patients with higher AC scores had lower serum iPTH levels and bone histomorphometry, suggestive of low bone activity and adynamic bone disease. Conversely, HD patients either without AC or with lower AC scores had similar serum iPTH levels and bone histomorphometry. In addition, during the recent ERA-EDTA Meeting in Barcelona, Asci et al. [4] showed that coronary artery calcification is associated with low bone activation frequency in 224 prevalent HD patients who underwent bone biopsy.
Interestingly, the pathogenesis of vascular calcification (VC) in chronic kidney disease has been extensively investigated [5]. Nowadays we know that VC is an active process, in which different bone regulatory proteins play a crucial role, because of their ability to induce or inhibit mineral deposition in the vessels. Considering the complexity of the VC process, it is no surprise that the article by Coen et al. [1] showed opposite results, compared to the previous studies.
In conclusion, we fully agree with the authors’ conclusions about the ‘special attention’ to be paid to HD patients with severe SHPT, using correct bath calcium concentrations, reducing oral calcium intake and prescribing vitamin D receptor activators with minimal effects on serum calcium and phosphate levels.
Conflict of interest statement. None declared.
Department of Nephrology Renal Division, S. Paolo Hospital University of Milan Italy
References
- Coen G, Manni M, Mantella D, et al. Are PTH serum levels predictive of coronary calcifications in haemodialysis patients? Nephrol Dial Transplant (2007) June 27 [Epub ahead of print].
- 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] - 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] - 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.
- Cozzolino M, Brancaccio D, Gallieni M, Slatopolsky E. Pathogenesis of vascular calcification in chronic kidney disease. Kidney Int (2005) 68:429–436.[CrossRef][Web of Science][Medline]
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