Article

Reducing the Burden of Cardiovascular Calcification in Patients with Chronic Kidney Disease

Department of Medicine, University of Texas Health Sciences Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.
Journal of the American Society of Nephrology (Impact Factor: 9.34). 12/2005; 16 Suppl 2(11):S95-102. DOI: 10.1681/ASN.2005060666
Source: PubMed

ABSTRACT

Patients with chronic kidney disease (CKD) have a higher burden of atherosclerotic coronary artery disease compared with age- and gender-matched individuals with normal renal function. Cardiovascular calcification (CVC), a marker of atherosclerosis, is also more prevalent in these patients and is associated with serious clinical consequences. The pathogenesis of CVC is complex and includes factors that promote calcification and others that inhibit calcification. Thus, multiple therapeutic interventions should be used simultaneously to reduce the burden of calcification in patients with CKD. Thus far, interventional attempts have focused on curtailing the effects of factors that promote calcification such as management of known traditional factors for atherosclerotic coronary artery disease and on adopting specific approaches to normalize mineral metabolism, deliver adequate dialysis, and control serum cholesterol level. By contrast, interventions that may bolster the effects of inhibitors of calcification have not yet been studied well but are beginning to attract attention. Ideally, the goal of interventions is not only to slow or halt progression of calcification but also to reverse pre-existing calcification. Whether this goal is achievable is not currently known. This review examines the potential of various therapeutic interventions in reducing the CVC burden in patients with CKD. Moreover, the review is intended to stimulate more research in this area because the efficacy of these interventions has not been examined in controlled clinical trials.

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    ABSTRACT: Progression of coronary artery calcification (CAC) has been described in hemodialysis patients, and severe CAC has been associated with the occurrence of cardiovascular events in this population. Little information is available regarding peritoneal patients. To prospectively evaluate peritoneal dialysis patients in order to identify the variables associated with the rate of CAC progression, as well as to determine the impact that baseline CAC has on clinical outcomes over a 1-year follow-up period. Using multislice coronary tomography, calcium scores were estimated at baseline and after 12 months in 49 peritoneal dialysis patients. Patients with and without CAC progression were compared with respect to clinical characteristics and biochemical variables, including lipid profile, parameters of mineral metabolism, and markers of inflammation. Cardiovascular events, hospitalizations, and all-cause mortality were recorded. At baseline, 29 patients (59%) presented CAC and a median calcium score of 234.7 (range 10.3-2351) Agatston units. Progression of CAC was observed in 13 patients (43%) who, in comparison with those presenting no CAC progression, were older, presented higher baseline calcium scores, and had higher mean glucose levels, lower mean high density lipoprotein cholesterol levels, and more months using low calcium peritoneal solution. We also observed a trend toward more often presenting with a history of hypertension, exhibiting more hyperphosphatemic and hyperglycemic events, and having lower albumin levels. In multiple logistic regression, only baseline calcium score was independently associated with progression of CAC. A shorter cardiovascular event-free time and a trend toward lower survival rates were observed in the group with CAC. Hospitalization event-free time did not differ between the groups. Determining CAC provides important prognostic data in peritoneal dialysis patients. Baseline calcium score and disturbances in glucose, mineral, and lipid metabolism were indicative of higher risk of CAC progression in this population.
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    Preview · Article · Jul 2006 · Journal of the American Society of Nephrology
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