Treatment Protocol for Controlling Bone Metabolism Parameters in Hemodialysis Patients

Abnormal mineral metabolism and severe secondary hyperparathyroidism play a key role in the pathophysiology of skeletal and extraskeletal calcification and are associated with increased morbidity and mortality among hemodialysis (HD) patients (Block GA et al., 1998, 2004; Ganesh et al., 2001; London GM et al., 2003). As a result of these findings, the National Kidney Foundation introduced guidelines in 2003 on controlling parathyroid hormone (PTH), calcium (Ca), phosphorous (P) and calcium-phosphorous ion product (CaxP) in these patients (National Kidney Foundation-Kidney Disease Outcomes and Quality Initiative, 2003). However, in spite of the publication of the K/DOQI guidelines, most HD patients remained outside the recommended targets (Al Aly et al., 2004; Arenas et al., 2006; Lorenzo et al., 2006; Maduell et al., 2005). Historically, Ca-containing phosphate binders and vitamin D have provided the main strategies for reducing P and PTH levels (Slatopolsky et al., 1986). However, the overuse of Ca-containing phosphate binders and active vitamin D can result in hypercalcemia, high CaxP level and Ca overload, which may accelerate vascular disease and hasten death. These side effects potentially require temporary cessation of vitamin D and a reduction in Ca-containing binder administration. This cycle results in a temporary worsening of secondary hyperparathyroidism, allowing bone disease progression (Block et al., 1998, 2000; Johnson et al., 2002; Moe et al., 2003). Hence, new treatment strategies are required (Jindal et al., 2006; Moe et al., 2009;). Since 2006, two new drugs, paricalcitol and cinacalcet, have been available in daily clinical practice for secondary hyperparathyroidism treatment. Paricalcitol is a vitamin D metabolite that has some advantages over calcitriol, the standard form of vitamin D used worldwide. Paricalcitol suppresses PTH faster than calcitriol (Sprague et al., 2001), and may have a lesser Ca and P intestinal absorption capacity, with smaller increases in Ca and P serum (Llach et al., 2001). Patients who receive paricalcitol may also have a significant survival advantage over those who receive calcitriol (Teng et al., 2003). Despite these advantages, the occurrence of hypercalcemia and high CaxP, when high doses of paricalcitol are used, is not unusual (Goodman, 2001; Martin & Gonzalez, 2001).