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Association of serum calcitonin with coronary artery disease in individuals with and without chronic kidney disease

  • Nephrology - Original Paper
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Abstract

Background

Cardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD). Recent data implicate disordered bone and mineral metabolism, including changes in serum levels of calcium, phosphate, parathyroid hormone (PTH), vitamin D, fibroblast growth factor-23 (FGF-23), and fetuin A, as novel risk factors for arterial calcification. The potential role of calcitonin, another hormonal regulator of mineral and bone metabolism, has not been studied in detail.

Materials and methods

We investigated the link between serum calcitonin and the total burden of coronary artery disease (CAD) using the validated Gensini score, in a cross-sectional study of 88 patients with estimated GFR (eGFR) between 46 and 87 ml/min/1.73 m² who underwent coronary angiography. We evaluated the associations between serum calcitonin, minerals (calcium, phosphate), calcium × phosphate product, and other factors that regulate mineral metabolism (intact PTH, 25-OH-vitamin D, FGF-23, and fetuin A) and the severity of CAD.

Results

The mean serum calcitonin was 11.5 ± 7.8 pg/ml. In univariate analysis, the Gensini CAD severity score correlated significantly with male gender, eGFR, and serum levels of 25-OH-vitamin D, iPTH, FGF-23, fetuin A, and calcitonin (R = 0.474, P = 0.001 for the latter). In multivariate analysis adjusted for calcium, phosphate, 25-OH-vitamin D, iPTH, FGF 23, fetuin A, and calcitonin, only calcitonin (β = 0.20; P = 0.03), FGF-23, fetuin A, and 25-OH-vitamin D emerged as independent predictors of Gensini score. In the second step, we adjusted for the presence of traditional risk factors, proteinuria, and GFR. After these adjustments, the FGF-23 and fetuin A remained statistically significant predictors of the Gensini score, while calcitonin did not.

Conclusions

Our study suggests that, in addition to other well-known components of mineral metabolism, increased calcitonin levels are associated with greater severity of CAD. However, this relation was not independent of traditional and nontraditional cardiovascular risk factors. Longitudinal studies in larger populations including patients with more advanced CKD are needed.

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References

  1. Foley RN, Parfrey PS, Sarnak MJ (1998) Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis 32(5 Suppl 3):S112–S119

    Article  PubMed  CAS  Google Scholar 

  2. London GM, Guerin AP, Marchais SJ, Metivier F, Pannier B, Adda H (2003) Arterial media calcification in end-stage renal disease: impact on all-cause and cardiovascular mortality. Nephrol Dial Transplant 18(9):1731–1740

    Article  PubMed  Google Scholar 

  3. Covic A, Kanbay M, Voroneanu L et al (2010) Vascular calcification in chronic kidney disease. Clin Sci (Lond) 119(3):111–121

    Article  CAS  Google Scholar 

  4. Mizobuchi M, Towler D, Slatopolsky E (2009) Vascular calcification: the killer of patients with chronic kidney disease. J Am Soc Nephrol 20(7):1453–1464

    Article  PubMed  CAS  Google Scholar 

  5. Kanbay M, Nicoleta M, Selcoki Y et al (2010) Fibroblast growth factor 23 and fetuin A are independent predictors for the coronary artery disease extent in mild chronic kidney disease. Clin J Am Soc Nephrol 5(10):1780–1786

    Article  PubMed  CAS  Google Scholar 

  6. Goodman HM (2003) Basic medical endocrinology, 3rd edn. Academic Press, Waltham

  7. Mancia G, De Backer G, Dominiczak A et al (2007) 2007 ESH-ESC practice guidelines for the management of arterial hypertension: ESH-ESC task force on the management of arterial hypertension. J Hypertens 25(9):1751–1762

    Article  PubMed  CAS  Google Scholar 

  8. Gensini GG (1983) A more meaningful scoring system for determining the severity of coronary heart disease. Am J Cardiol 51(3):606

    Google Scholar 

  9. Jacob MP, Moura AM, Tixier JM et al (1987) Prevention by calcitonin of the pathological modifications of the rabbit arterial wall induced by immunization with elastin peptides: effect on vascular smooth muscle permeability to ions. Exp Mol Pathol 46(3):345–356

    Article  PubMed  CAS  Google Scholar 

  10. Borchhardt KA, Horl WH, Sunder-Plassmann G (2005) Reversibility of ‘secondary hypercalcitoninemia’ after kidney transplantation. Am J Transplant 5(7):1757–1763

    Article  PubMed  Google Scholar 

  11. Niccoli P, Brunet P, Roubicek C et al (1995) Abnormal calcitonin basal levels and pentagastrin response in patients with chronic renal failure on maintenance hemodialysis. Eur J Endocrinol 132(1):75–81

    Article  PubMed  CAS  Google Scholar 

  12. Akan B, Bohmig G, Sunder-Plassmann G, Borchhardt KA (2009) Prevalence of hypercalcitoninemia in patients on maintenance dialysis referred to kidney transplantation. Clin Nephrol 71(5):538–542

    PubMed  CAS  Google Scholar 

  13. Martinez ME, Miguel JL, Gomez P et al (1983) Plasma calcitonin concentration in patients treated with chronic dialysis: differences between hemodialysis and CAPD. Clin Nephrol 19(5):250–253

    PubMed  CAS  Google Scholar 

  14. Canavese C, Barolo S, Gurioli L et al (1998) Correlations between bone histopathology and serum biochemistry in uremic patients on chronic hemodialysis. Int J Artif Organs 21(8):443–450

    PubMed  CAS  Google Scholar 

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Correspondence to Mehmet Kanbay.

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Kanbay, M., Wolf, M., Selcoki, Y. et al. Association of serum calcitonin with coronary artery disease in individuals with and without chronic kidney disease. Int Urol Nephrol 44, 1169–1175 (2012). https://doi.org/10.1007/s11255-011-0076-x

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  • DOI: https://doi.org/10.1007/s11255-011-0076-x

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