A 55-year-old woman with stage IV chronic kidney disease due to type 2 diabetes mellitus comes to the office for a follow-up visit. Blood pressure is 140/90 mm Hg and pulse is 78/min. BMI is 31 kg/m². Laboratory results are as follows: The patient's serum phosphorus has been persistently elevated despite strict dietary phosphate restriction. Treatment with sevelamer is initiated. This medication reduces the serum phosphorus level by which of the following mechanisms?

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Chronic kidney disease (CKD) often causes hyperphosphatemia due to the impaired ability of the kidneys to excrete phosphorus. Hyperphosphatemia is thought to be the inciting event in the onset of CKD-related mineral bone disorder. Elevated blood phosphate triggers the release of fibroblast growth factor 23 from bone, which lowers calcitriol production and intestinal calcium absorption. Reduced circulating calcium, along with hyperphosphatemia, leads to secondary hyperparathyroidism. Dietary phosphorus restriction is recommended for patients with CKD. However, oral phosphate binders are usually needed if dietary restriction is not sufficient to lower phosphate levels. Phosphate binders can be calcium containing (eg, calcium carbonate/acetate) or non-calcium containing (eg, sevelamer, lanthanum). Sevelamer is a nonabsorbable anion-exchange resin that binds intestinal phosphate to reduce systemic absorption. The resulting complex is eliminated in the feces. (Choice A) Vitamin D receptor antagonists are largely experimental compounds that have been considered for the treatment of Paget disease of bone. Most patients with CKD benefit from vitamin D supplementation due to decreased renal formation of 1,25-dihydroxyvitamin D. (Choices C, D, and F) Parathyroid hormone induces internalization and destruction of type IIa sodium/phosphate cotransporters (NPT2) in the proximal renal tubule. NPT2 gene expression is downregulated by fibroblast growth factor 23. These processes lead to decreased transcellular transport (and therefore decreased reabsorption) of phosphate in the renal tubules. (Choice E) Parathyroid hormone functions to reduce phosphate reabsorption by the kidney; reduced secretion would worsen, not correct, hyperphosphatemia. Sevelamer reduces circulating serum phosphorus by blocking intestinal absorption, which helps to mitigate secondary hyperparathyroidism. Educational objective: Chronic kidney disease can cause hyperphosphatemia due to decreased renal excretion of phosphorus. Dietary phosphorus restriction is recommended, but oral phosphate binders are often needed. Sevelamer is a nonabsorbable anion-exchange resin that binds intestinal phosphate to reduce absorption. __________ References: Sevelamer carbonate: a review in hyperphosphataemia in adults with chronic kidney disease. (http://www.ncbi.nlm.nih.gov/pubmed/24811546)

A 55-Year-Old Woman with Stage IV Chronic Kidney Disease Due