Secondary hyperparathyroidism (SHPT) is common in patients receiving maintenance hemodialysis (MHD) and is associated with adverse outcomes. Currently, SHPT is managed by reducing circulating levels of phosphate with oral binders and parathyroid hormone (PTH) with vitamin D analogs and/or the calcimimetic Cinacalcet (CC).
This article provides a brief overview of the pathogenesis of SHPT in CKD, with particular attention paid to the main molecular regulators that are affected by calcimimetics. Etelcalcetide (EC) is a new second-generation calcimimetic administered intravenously (IV) at the end of a hemodialysis treatment session, effectively reduces PTH in clinical trials when given thrice weekly. Apart from improving drug adherence, EC has proven to be more effective in lowering PTH when compared to CC, with an acceptable and comparable safety profile. Additional clinical effects include reductions in circulating levels of phosphate and FGF-23 and an improved profile of markers of bone turnover. However, despite being administered IV, EC appears to be associated with rates of nausea and vomiting comparable to those of CC. It is likely that EC can be used in the treatment of MHD patients with severe SHPT or with hypercalcemia or hyperphosphatemia receiving active metabolites of vitamin D. However, its use should be at least partially constrained by consideration of the risk of hypocalcemia and resultant prolonged electrocardiographic QT intervals in vulnerable patients. Because of its effectiveness as a PTH-reducing agent administered in the dialysis unit, EC represents a potentially promising new therapeutic approach for the treatment of SHPT in HD patients. In this article, we briefly summarize the pathogenesis of sHPT in CKD and describe clinical data of the new intravenous third-generation calcimimetic EC.

Keywords: etelcalcetide, calcimimetic, dialysis, secondary hyperparathyroidism, chronic kidney disease