Chronic kidney disease is one of the most rapidly increasing chronic diseases in the United States. More than 20 million US adults have an estimated glomerular filtration rate of less than 60 mL/min/1.73m2, which represents loss of more than half of normal kidney function.1 Disturbances in phosphorus, calcium, and vitamin D metabolic pathways develop early during chronic kidney disease and eventually affect most patients during the course of their disease.2 Data from cell culture and animal models suggest that mineral metabolism disorders might play a causal role in the development of vascular calcification, arterial stiffness, and ventricular hypertrophy.3- 5 Biomarker studies of serum concentrations of phosphorus, calcium, and parathyroid hormone provide complementary data for evaluating whether these metabolic pathways might contribute to the development of clinical disease outcomes in humans.
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