Skip to main content
Erschienen in: International Urology and Nephrology 4/2012

01.08.2012 | Nephrology - Original Paper

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

verfasst von: Mehmet Kanbay, Myles Wolf, Yusuf Selcoki, Yalcin Solak, Mustafa Ikizek, Sema Uysal, Liviu Segall, Ferah Armutcu, Beyhan Eryonucu, Murat Duranay, David Goldsmith, Adrian Covic

Erschienen in: International Urology and Nephrology | Ausgabe 4/2012

Einloggen, um Zugang zu erhalten

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.
Literatur
1.
Zurück zum Zitat 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–S119PubMedCrossRef 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–S119PubMedCrossRef
2.
Zurück zum Zitat 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):1731–1740PubMedCrossRef 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):1731–1740PubMedCrossRef
3.
Zurück zum Zitat Covic A, Kanbay M, Voroneanu L et al (2010) Vascular calcification in chronic kidney disease. Clin Sci (Lond) 119(3):111–121CrossRef Covic A, Kanbay M, Voroneanu L et al (2010) Vascular calcification in chronic kidney disease. Clin Sci (Lond) 119(3):111–121CrossRef
4.
Zurück zum Zitat Mizobuchi M, Towler D, Slatopolsky E (2009) Vascular calcification: the killer of patients with chronic kidney disease. J Am Soc Nephrol 20(7):1453–1464PubMedCrossRef Mizobuchi M, Towler D, Slatopolsky E (2009) Vascular calcification: the killer of patients with chronic kidney disease. J Am Soc Nephrol 20(7):1453–1464PubMedCrossRef
5.
Zurück zum Zitat 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):1780–1786PubMedCrossRef 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):1780–1786PubMedCrossRef
6.
Zurück zum Zitat Goodman HM (2003) Basic medical endocrinology, 3rd edn. Academic Press, Waltham Goodman HM (2003) Basic medical endocrinology, 3rd edn. Academic Press, Waltham
7.
Zurück zum Zitat 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):1751–1762PubMedCrossRef 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):1751–1762PubMedCrossRef
8.
Zurück zum Zitat Gensini GG (1983) A more meaningful scoring system for determining the severity of coronary heart disease. Am J Cardiol 51(3):606 Gensini GG (1983) A more meaningful scoring system for determining the severity of coronary heart disease. Am J Cardiol 51(3):606
9.
Zurück zum Zitat 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):345–356PubMedCrossRef 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):345–356PubMedCrossRef
10.
Zurück zum Zitat Borchhardt KA, Horl WH, Sunder-Plassmann G (2005) Reversibility of ‘secondary hypercalcitoninemia’ after kidney transplantation. Am J Transplant 5(7):1757–1763PubMedCrossRef Borchhardt KA, Horl WH, Sunder-Plassmann G (2005) Reversibility of ‘secondary hypercalcitoninemia’ after kidney transplantation. Am J Transplant 5(7):1757–1763PubMedCrossRef
11.
Zurück zum Zitat 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):75–81PubMedCrossRef 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):75–81PubMedCrossRef
12.
Zurück zum Zitat 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):538–542PubMed 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):538–542PubMed
13.
Zurück zum Zitat 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):250–253PubMed 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):250–253PubMed
14.
Zurück zum Zitat 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):443–450PubMed 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):443–450PubMed
Metadaten
Titel
Association of serum calcitonin with coronary artery disease in individuals with and without chronic kidney disease
verfasst von
Mehmet Kanbay
Myles Wolf
Yusuf Selcoki
Yalcin Solak
Mustafa Ikizek
Sema Uysal
Liviu Segall
Ferah Armutcu
Beyhan Eryonucu
Murat Duranay
David Goldsmith
Adrian Covic
Publikationsdatum
01.08.2012
Verlag
Springer Netherlands
Erschienen in
International Urology and Nephrology / Ausgabe 4/2012
Print ISSN: 0301-1623
Elektronische ISSN: 1573-2584
DOI
https://doi.org/10.1007/s11255-011-0076-x

Weitere Artikel der Ausgabe 4/2012

International Urology and Nephrology 4/2012 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Chronische Verstopfung: „Versuchen Sie es mit grünen Kiwis!“

22.05.2024 Obstipation Nachrichten

Bei chronischer Verstopfung wirken Kiwis offenbar besser als Flohsamenschalen. Das zeigen die Daten aus einer randomisierten Studie, die der Gastroenterologe Oliver Pech beim Praxis-Update vorstellte.

Blutdrucksenkung könnte Uterusmyome verhindern

Frauen mit unbehandelter oder neu auftretender Hypertonie haben ein deutlich erhöhtes Risiko für Uterusmyome. Eine Therapie mit Antihypertensiva geht hingegen mit einer verringerten Inzidenz der gutartigen Tumoren einher.

„Jeder Fall von plötzlichem Tod muss obduziert werden!“

17.05.2024 Plötzlicher Herztod Nachrichten

Ein signifikanter Anteil der Fälle von plötzlichem Herztod ist genetisch bedingt. Um ihre Verwandten vor diesem Schicksal zu bewahren, sollten jüngere Personen, die plötzlich unerwartet versterben, ausnahmslos einer Autopsie unterzogen werden.

Hirnblutung unter DOAK und VKA ähnlich bedrohlich

17.05.2024 Direkte orale Antikoagulanzien Nachrichten

Kommt es zu einer nichttraumatischen Hirnblutung, spielt es keine große Rolle, ob die Betroffenen zuvor direkt wirksame orale Antikoagulanzien oder Marcumar bekommen haben: Die Prognose ist ähnlich schlecht.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.