From Heartwire
Serum Phosphorous, Kidney Function Predict CACReed Miller
November 13, 2009 — High levels of serum phosphorus and reduced kidney function at levels usually considered normal independently predict coronary artery calcification (CAC) in addition to traditional cardiovascular disease risk factors, according to a new study published online November 5, 2009, in the Clinical Journal of the American Society of Nephrology [1].
"These data shed light on a nontraditional mechanism for CVD, which may help to explain unexpected responses to traditional therapies in patients with [chronic kidney disease] CKD," Dr Katherine Tuttle (Providence Medical Research Center, Seattle, WA) and Dr Robert Short (Washington State University, Spokane) explain.
The 883-patient study, part of the Spokane Heart Study, found that each 1-mg/dL increase in serum phosphorus level, which is associated with loss of kidney function, imparted odds ratios for CAC incidence of 1.61 and CAC prevalence of 1.54, an impact similar to that of other traditional risk factors.
The study enrolled 883 healthy people with no known cardiovascular disease or major comorbidities between 1994 and 2003. The subjects underwent a battery of tests, including CAC testing with electron-beam computed tomography, every two years for at least six years.
CAC was found in 28% of patients upon entry into the study, more commonly in patients who were male and had hypertension and histories of smoking or family members with cardiovascular disease; levels of serum phosphorus and estimated glomerular filtration rate (eGFR) did not differ by CAC status. During the six years of follow-up, the prevalence and incidence of CAC increased progressively, so the overall prevalence by the end of the study was 50%.
Neither eGFR nor serum phosphorous differed by CAC presence or absence at baseline, but multivariate models showed that the independent predictors of CAC over time were greater baseline CAC scores, higher serum phosphorous levels, lower eGFR levels, and traditional cardiovascular disease risk factors.
Calcification is typically part of atherosclerotic disease, but in patients with decreased renal function, calcium chiefly deposits in the media and internal elastic lamina of the arterial walls, eventually leading to advancing sclerosis in the coronary arteries and throughout the circulation, Tuttle and Short explain. Animal models show that hyperphosphatemia is a key contributor to vascular calcification. High serum phosphorus leading to aortic calcification in experimental animals can be corrected by phosphate-binding drugs or dietary restriction. Furthermore, "a growing series of observations in humans are consistent with experimental models, in that higher serum phosphorus has been reported to predict CAC and CVD events in people without clinically apparent kidney disease," they state.
"Observational human data combined with experimental studies make a case for testing effects of treatments that reduce phosphate on CVD outcomes in patients who are in earlier stages of CKD or perhaps even in those who do not have CKD but have CAC," the authors explain. "On the basis of the concept that calcification is central to mechanisms of CVD, treatment strategies that minimize tissue deposition of calcium (eg, reduced phosphate diet and/or noncalcemic phosphate binders) are of particular interest."
http://www.medscape.com/viewarticle/712333
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