Etelcalcetide is a new calcimimetic indicated for the treatment of secondary hyperparathyroidism (SHPT) in dialysis patients. Etelcalcetide efficacy in SHPT has been ascertained only in randomized controlled trials. This multicenter study was carried out in “real world” setting that is different from randomized controlled trials (RCTs) to (1) evaluate the effectiveness of etelcalcetide in SHPT, (2) to assess calcium, phosphorus, alkaline phosphatase changes, (3) to register gastrointestinal side effects. Data were collected from twenty-three dialysis units with n = 1190 patients on the charge. From this cohort, n = 168 (14%) patients were on treatment with etelcalcetide, and they were evaluated for statistics. A median weekly dose of etelcalcetide was 15 mg (7.5–45 mg). Patients were either naïve (33%) or switched from cinacalcet to obtain better control of SHPT with reduced side effects or pills burden. Serum parathyroid hormone (PTH) declined over time from a median value of 636 pg/mL to 357 pg/mL. The median time for responders (intact PTH (iPTH) range: two to nine times the upper normal limit) was 53 days; the percentage of responders increased (from baseline 27% to 63%) being similar in switched-patients and naïve-patients. Few patients had symptomatic hypocalcemia requiring etelcalcetide withdrawal (four cases (3%) at 30-day control, two cases (2%) at 60-day, one case (1%) at 90-day control). Side effects with etelcalcetide were lower (3–4%) than that registered during cinacalcet treatment (53%). Etelcalcetide is a new therapeutic option for SHPT with low side effects and pills burden. Etelcalcetide may improve adherence to therapy, avoiding unremitting SHP. It remains to be assessed whether etelcalcetide may reduce parathyroidectomy, vascular calcification, or mortality. Being etelcalcetide very potent in suppressing PTH levels, even in severe SHPT, future studies should evaluate the potential risk of more adynamic bone disease during long-term therapy.

Mortality rate among patients with stage five chronic kidney disease (CKD) maintained on hemodialysis (HD) is high. Although evidence suggests that use of Vitamin D Receptor Activators (VDRA) in CKD patients increases survival, few studies have examined the effect of VDRA in incident HD patients. The FARO-2 study evaluated the clinical outcome of VDRA therapy on mortality in incident HD patients. FARO-2 was a longitudinal epidemiological study performed on 568 incident HD patients followed prospectively from 26 dialysis centers over a 3-year period. Data were collected every 6 months using a questionnaire, obtaining clinical, biochemical and therapeutic parameters. Kaplan-Meier curves and Cox proportional hazard regression models were used to determine cumulative probability of time-to-death and adjusted hazard ratios. 568 patients (68% male) with an average age of 65.5 years were followed up. Mean dialysis duration at study entry was 3 months. VDRA use increased from 46% at 6 months to 54.7% at 36 months of follow-up (p = 0.08). No difference was observed in the presence of comorbid diseases at baseline in patients with and without VDRA therapy. Cumulative probability of survival at 24 months was 74.5% (95% CI: 70.2-78.3). Patients receiving VDRA therapy showed a significant increase in survival at 24 months (80.7%; 95% CI: 75.7-84.8) compared to those without (63.3%; 95% CI: 54.8-70.7, p <0.01). The presence of vascular disease, decreased hemoglobin, increased P and lack of VDRA treatment were significantly associated with an increased risk of mortality. Lack of VDRA treatment still remained significant as a predictor of mortality after adjusting for levels of PTH, P and Ca (HR = 2.16, 95% CI: 1.09-4.30, p = 0.03). Findings from FARO-2 indicate that in incident HD patients VDRA therapy was associated with increased survival.

Hypercalcaemia has been reported to occur in ∼1–4% of the general adult population, and in 0.5–3% of hospitalized adult patients [1]. Hypercalcaemia results when the entry of calcium (Ca) into the extracellular fluid exceeds excretion in the urine or deposition in bone. This occurs when there is accelerated bone resorption, excessive gastrointestinal absorption or decreased renal excretion of Ca. Under most pathologic conditions, hypercalcaemia results from increased skeletal resorption or intestinal absorption with normal or decreased renal excretion. In some disorders more than one mechanism may be involved. As an example, in primary hyperparathyroidism, elevated parathyroid hormone (PTH) levels increase bone resorption, tubular Ca reabsorption and, indirectly, intestinal Ca absorption (by increasing renal synthesis of calcitriol). Among all causes of hypercalcaemia, primary hyperparathyroidism and malignancy are the most common, accounting for >90% of cases [2].

The authors wish to make the following corrections to the previous publication

Denosumab, a fully human monoclonal antibody against the receptor activator of nuclear factor kappa B ligand (RANKL), has been approved for the prevention of skeletal-related events in metastatic solid tumor patients with bone metastases. As opposed to the bisphosphonates, denosumab is not excreted by the kidney, and renal function does not have a significant effect on denosumab pharmacokinetics or pharmacodynamics. Thus, dose adjustment is not required in patients with renal insufficiency. In contrast to the bisphosphonates, denosumab has not been documented to have nephrotoxic effects. However, it does share some toxicities with bisphosphonates, including hypocalcemia and osteonecrosis of the jaw. In this review, the warnings and recommendations for the use of denosumab in patients with renal insufficiency are discussed.