Introduction and Aims: Vascular calcifications (VC) are predictors of morbidity and mortality in patients on dialysis (ESRD-patients). VC and particularly coronary artery calcification (CAC) proceed over time. Ab- normal mineral metabolism as well as reduction of “protective” proteins (e.g. fetuin-A) are involved in progression of CAC. Rapid progression is regarded as additional factor responsible for morbidity and mortality. Determinants of CAC progression have not been evaluated in patients with kidney disease not undergoing dialysis (CKD-patients). This study assesses CAC progression and determinants in CKD-patients. Awareness of rate and potential determinants of CAC can allow early therapeutic interventions and expectantly hinder cardiovascular morbidity and mortality. Methods: Consecutive out-patients (age 18-70 years) with normal or reduced renal function (stage 3-5 CKD not on dialysis) were enrolled. Ex- clusion criteria were: symptomatic coronary disease; arrhythmia; myocardial infarction; diabetes. In patients with diabetes CAC progression is greater and independent of mineral metabolism and renal function. Serum cal- cium, phosphorus, parathyroid hormone, homocysteine, C-reactive protein, triglycerides, total cholesterol, high- and low-density lipoprotein cholesterol were serially measured. Fetuin-A was assessed at the entry and at the end of the study. CAC progression was detected by measuring total calcium score (TCS) with computed tomography. Follow-up lasted 24±4.2 months (mean±SE). Results: n.53 patients had CKD and 60 had normal renal function (NRF- patients). Patients with CAC were older with lower fetuin-A. TCS increased from 73±17 to 80±20 (mean±SE; p=NS) in NRF-patients and from 384±116 to 602±140 (mean±SE; p<0.01) in CKD-patients. Despite the majority of patients had normal concentration, phosphorus [O.R.=1.97 (1.14-3.41, 95% C.I.); p=0.015] correlated with CAC progression. N.11 CKD-patients, 45-70 years old, experienced fatal or not fatal cardiovascular event. All but one patient presented progression of CAC. In contrast, no event occurred in NRF-patients. Conclusions: CAC progression was prominent in CKD-patients and cor- related with serum phosphorus. Cardiovascular events were more frequent in CKD-patients. Studies are required to ascertain whether the attainment of serum phosphorus lower than that suggested by guidelines may reduce CAC progression, and ultimately mortality.
Determinants of coronary artery calcification progression in patients with chronic kidney disease not on dialysis
BATTAGLIA Y;
2007-01-01
Abstract
Introduction and Aims: Vascular calcifications (VC) are predictors of morbidity and mortality in patients on dialysis (ESRD-patients). VC and particularly coronary artery calcification (CAC) proceed over time. Ab- normal mineral metabolism as well as reduction of “protective” proteins (e.g. fetuin-A) are involved in progression of CAC. Rapid progression is regarded as additional factor responsible for morbidity and mortality. Determinants of CAC progression have not been evaluated in patients with kidney disease not undergoing dialysis (CKD-patients). This study assesses CAC progression and determinants in CKD-patients. Awareness of rate and potential determinants of CAC can allow early therapeutic interventions and expectantly hinder cardiovascular morbidity and mortality. Methods: Consecutive out-patients (age 18-70 years) with normal or reduced renal function (stage 3-5 CKD not on dialysis) were enrolled. Ex- clusion criteria were: symptomatic coronary disease; arrhythmia; myocardial infarction; diabetes. In patients with diabetes CAC progression is greater and independent of mineral metabolism and renal function. Serum cal- cium, phosphorus, parathyroid hormone, homocysteine, C-reactive protein, triglycerides, total cholesterol, high- and low-density lipoprotein cholesterol were serially measured. Fetuin-A was assessed at the entry and at the end of the study. CAC progression was detected by measuring total calcium score (TCS) with computed tomography. Follow-up lasted 24±4.2 months (mean±SE). Results: n.53 patients had CKD and 60 had normal renal function (NRF- patients). Patients with CAC were older with lower fetuin-A. TCS increased from 73±17 to 80±20 (mean±SE; p=NS) in NRF-patients and from 384±116 to 602±140 (mean±SE; p<0.01) in CKD-patients. Despite the majority of patients had normal concentration, phosphorus [O.R.=1.97 (1.14-3.41, 95% C.I.); p=0.015] correlated with CAC progression. N.11 CKD-patients, 45-70 years old, experienced fatal or not fatal cardiovascular event. All but one patient presented progression of CAC. In contrast, no event occurred in NRF-patients. Conclusions: CAC progression was prominent in CKD-patients and cor- related with serum phosphorus. Cardiovascular events were more frequent in CKD-patients. Studies are required to ascertain whether the attainment of serum phosphorus lower than that suggested by guidelines may reduce CAC progression, and ultimately mortality.
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
