De novo Development of Heart Valve Calcification in Incident Peritoneal Dialysis Patients

Background and Aims c valve calcification (VC) is a frequent complication in chronic kidney disease and is considered a risk factor for all-cause and cardiovascular mortality. However, little is known about the pathophysiology mechanisms that originate it and the factors associated with its development. We undertook this study to analyze the frequency and factors related to de novo development of mitral valve calcification (MVC) and aortic valve calcifications (AVC) in incident peritoneal dialysis (PD) patients. s pective cohort of 124 incident PD patients was studied. Demographic and clinical data were recorded and blood assayed at baseline and after 1 year of follow-up for calcium, phosphorus, glucose, urea, creatinine, cholesterol, triglycerides by spectrophotometry assay; high-sensitivity C-reactive protein (CRP) by immunoturbidimetric ultrasensitive assay, intact parathormone (iPTH) and osteocalcin by electrochemiluminescence, fetuin-A and osteoprotegerin by EDI-ELISA. Valve calcification was evaluated by M-mode bidimensional echocardiogram. s eight percent of patients were male, ages 43 ± 13 years; 51% were diabetic with 1.4 ± 1 months on PD. After 12.3 ± 1 months, 57 patients (46%) developed VC: AVC in 33 (57.8%), MVC in 15 (26.3%) and 9 (15.8%) patients in both valves. There was no correlation between AVC and MCV. In univariate logistic regression analysis, age, diabetes and elevated concentrations of OPG, iPTH and CRP were risk factors for development MVC. In multivariate analysis, only iPTH remained an independent risk factor as was also the case in AVC. sions iabetes, osteoprotegerin, parathormone and C-reactive protein are risk factors related to de novo development of MVC and iPTH for AVC in incident dialysis patients.