title: Serum calcitonin and endothelial dysfunction in chronic kidney disease: a novel risk factor?
abstract: BACKGROUND
  Endothelial dysfunction (ED) is highly prevalent in patients with CKD. The relationship between ED and calcitonin has not been demonstrated before in CKD patients.
  
  
  METHODS
  The study included non-diabetic CKD patients not on dialysis. Demographic data (age, gender, comorbidities, current drug therapy, smoking status, weight, and height) were collected from the individual charts in the hospital's electronic database. After overnight fasting, laboratory measurements including serum calcitonin levels were performed in all patients. A single observer who was blinded to the results of the study assessed ED by measurement of flow-mediated dilatation (FMD).
  
  
  RESULTS
  In total, 84 CKD patients (41 men, age 45.1 ± 13.3 years) were included. Thirty-seven patients had stage 3 and 47 patients had stage 4 CKD. Patients with calcitonin levels above the median had lower FMD (6.87 ± 0.58 vs. 7.23 ± 0.66, P = 0.008) when compared with patients with calcitonin levels below the median. None of the other demographic, laboratory and clinical parameters was different between the two groups. In multivariate regression analysis, serum calcitonin (P = 0.01), fetuin-A (P < 0.001), high-sensitive C-reactive protein (P < 0.001), and hemoglobin (P = 0.004) were independently associated with FMD.
  
  
  CONCLUSIONS
  Our present study demonstrated for the first time that serum calcitonin is independently related with ED. This finding deserves further experimental and clinical exploration, in order to elucidate whether calcitonin is an innocent bystander or has a pathophysiologic relationship with ED in patients with CKD.
authors.affiliation: Department of Medicine, Division of Nephrology, Kayseri Training and Research Hospital, Alparslan Mahallesi, Umit sokak, No:25/14, Melikgazi, Kayseri, Turkey. drkanbay@yahoo.com
authors.forename: Mehmet
authors.initials: M
authors.lastname: Kanbay
authors.forename: Mahmut Ilker
authors.initials: MI
authors.lastname: Yilmaz
authors.forename: Baris
authors.initials: B
authors.lastname: Afsar
authors.forename: Mutlu
authors.initials: M
authors.lastname: Saglam
authors.forename: Emin Ozgur
authors.initials: EO
authors.lastname: Akgul
authors.forename: Tuncer
authors.initials: T
authors.lastname: Cayci
authors.forename: Kayser
authors.initials: K
authors.lastname: Caglar
authors.forename: Hilmi Umut
authors.initials: HU
authors.lastname: Unal
authors.forename: Mahmut
authors.initials: M
authors.lastname: Gok
authors.forename: Abdulgaffar
authors.initials: A
authors.lastname: Vural
authors.forename: Adrian
authors.initials: A
authors.lastname: Covic
mesh_terms: D000328:Adult; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002097:C-Reactive Protein / Q000378:metabolism; D002116:Calcitonin / Q000097:blood*; D016009:Chi-Square Distribution; D004108:Dilatation, Pathologic / Q000000981:diagnostic imaging; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012039:Regional Blood Flow; D051436:Renal Insufficiency, Chronic / Q000097:blood* / Q000503:physiopathology*; D012307:Risk Factors; D018709:Statistics, Nonparametric; D014463:Ultrasonography; D060749:alpha-2-HS-Glycoprotein / Q000378:metabolism
chemical_list: D006454:Hemoglobins; D060749:alpha-2-HS-Glycoprotein; D002116:Calcitonin; D002097:C-Reactive Protein