Hyperphosphatemia is a common feature in patients with chronic kidney disease (CKD), especially in those with end-stage renal disease (ESRD). Commonly, high serum phosphate levels are observed only in later stages of CKD. The control of hyperphosphatemia plays a key role in the management of CKD patients. However, the optimal range for serum phosphate levels in CKD patients is still controversial. Currently, phosphate binders are the only medications available to reduce elevated serum phosphate levels in patients with ESRD receiving hemodialysis. Tenapanor, an inhibitor of gastrointestinal sodium/hydrogen exchanger 3 (NHE3), acts via a non-phosphate-binding mechanism, reducing paracellular phosphate transport in the intestine. Has tenapanor the potential to improve management of mineral bone disorder in CKD?
Keywords: Chronic kidney disease; Hyperphosphatemia; Phosphate binders; Sodium/hydrogen exchanger 3 (NHE3) inhibitors; Tenapanor; Vascular calcification.
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