Progression of Coronary Artery Calcification in Predialysis Patients

Abstract

Background: In patients on dialysis coronary artery calcification (CAC) rapidly proceeds due to impaired mineral metabolism and/or exogenous calcium load. Progression has not been assessed in patients with chronic kidney disease not yet requiring dialysis (CKD patients). In this study, rate and determinants of CAC progression have been evaluated in CKD patients who are exposed to minor derangement of mineral metabolism and calcium load. Methods: Consecutive patients were enrolled. Exclusion criteria were: symptomatic coronary disease, arrhythmia, myocardial infarction, and diabetes. Serum calcium, phosphorus, parathyroid hormone, homocysteine, C-reactive protein, triglycerides, total cholesterol, high- and low-density lipoprotein cholesterol were serially measured. Fetuin-A was assessed at entry into the study. CAC progression was detected by measuring total calcium score (TCS) with computed tomography. Initial and final scans were obtained. Predictive factors of progression were investigated. Results: Fifty-three patients had CKD (stage 3–5 CKD; K-DOQI classification) not yet requiring dialysis, and 60 patients had normal renal function (NRF patients). Follow-up lasted 24 ± 4.2 months (mean ± SE). Patients with CAC were older with lower serum 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. Serum phosphorus [OR = 1.97 (1.14–3.41, 95% CI); p = 0.015] was the only variable that was associated with CAC progression. Cardiovascular events occurred in CKD patients with CAC. Conclusion: CAC progression was prominent in CKD patients and correlated with serum phosphorus. Fatal and nonfatal cardiovascular events were more frequent in CKD patients. Studies are required to ascertain whether the attainment of serum phosphorus concentration lower than that suggested by current guidelines may reduce CAC progression and ultimately mortality.

Associations among time-average mineral values, mortality and cardiovascular events in hemodialysis patients

“…12 Coronary artery calcification is one of the reasons why hyperphosphatemia, hypercalcemia lead to cardiovascular events and mortality. 5,6,[17][18][19][20] However, after multivariate adjustment, the AHRs for mortality according to different categories of time average mineral values sorted by K/DOQI guidelines demonstrated no survival difference among all mineral values in our study. This conclusion is not similar to previous studies.…”

“…[1][2][3][4] Coronary artery calcification might be explanatory. 5,6 Therefore, Kidney Disease Outcomes Quality Initiative (K/DOQI) provides the target ranges of mineral values (Ca, P, PTH). They set target range of serum phosphate, calcium, intact parathyroid hormone and calcium-phosphorus product as 3.5-5.5 mg/dL, 8.4-9.5 mg/dL, 150-300 pg/mL and less than 55, respectively.…”

Progression of Coronary Artery Calcification and Thoracic Aorta Calcification in Kidney Transplant Recipients

“…Studies in healthy adults (53) and CKD patients (54) already observed an association of higher phosphatemia with atherosclerosis and vascular calcification. Russo et al established in a cohort of predialysis patients that higher phosphorus levels were associated with CAC progression (55). Another study performed in CKD patients observed an association between higher phosphorus levels and mortality (56).…”

Pulse Pressure and Presence of Coronary Artery Calcification

“…The disease progresses rapidly and is associated with fatal and nonfatal cardiovascular events (4,5). It is likely that in CKD patients, who frequently die from coronary heart disease before dialysis initiation, CAC is an important risk factor for cardiovascular events as in patients on dialysis (ESRD patients) (6 -9).…”