SP528CINACALCET IN A ONE CENTER PERITONEAL DIALYSIS PATIENTS: WHAT COULD WE EXPECT?

Abstract

Introduction and Aims: Mineral Bone Disease (MBD) has been largely studied in patients (pts) with Chronic Kidney Disease (CKD). The secondary hyperparathyroidism (SH) is the target of several therapeutic strategies, including the use of cinacalcet, which has improved the CKD-MBD outcomes. However, most studies were done only in hemodialysis pts, with few data from Peritoneal Dialysis (PD) pts. The aim of our study was to evaluate the effectiveness of cinacalcet in SH in a one-center dialysis peritoneal pts. Methods: We perform a retrospective study in a single peritoneal dialysis Unity in Portugal, based on the study of all 112 incident pts admitted during 5 years (yrs) in a PD program. We studied a cohort of 29 pts with moderate to severe secondary hyperparathyroidism (SH) who were treated with cinacalcet and we analyze demographic, clinical, laboratory parameters, including PTHi levels before and after cinacalcet therapy. We analyse the duration of cinacalcet therapy, maximum tolerated doses, effectiveness and safety, including the adverse effects. Results: Median age was 46,13±15,8 yrs; 15 (51,7%) were men, 6 (20,7%) pts had diabetes and the body mass index (BMI) was 26,09±5,15 Kg/m2; the pts were under PD at 29,86±16,72 months; all 29 patients were treated with cinacalcet for 12,39±13,47 months. The minimum doses was 15 mg/day and the maximum doses was 90 mg/day (mean 45 mg/day). About 70% of pts showed adverse gastrointestinal effects with higher cinacalcet doses; 65,5% of pts were treated with DP solutions with low calcium levels (1,25 mmol/L) and 34,5% with DP solutions containing calcium at 1,75 mmol/L; 26 (89,7%) of pts were under treatment with vitamin D analogs and phosphorus binders. The laboratorial levels at the beginning of cinacalcet therapy were: PTHi: 1135,81±472,46 pg/mL; Calcium: 9,07 ±0,83 mg/dL; Phosphorus: 5,14 ±0,82 mg/dL and nPCR: 1,02±0,27 g/kg/day. The last laboratorial follow up under cinacalcet therapy was: PTHi: 1131,926 ±584,88 pg/mL; Calcium: 9,16 ±0,84 mg/dL; Phosphorus: 5,92 ±0,99 mg/dL and nPCR: 0,95±0,23 g/Kg/day. At the last follow up 22 (81,5%) pts had PTHi levels higher than 600 pg/mL despite cinacalcet therapy at maximum tolerated doses. The Phosphorus levels were increasing during PD (p 0,03) but nPCR was similar to the value at the begining of PD. We don't identify deaths, bone fractures or increasing in the number of hospitalizations. Conclusions: Cinacalcet was a safe but not effective therapy in moderate to severe HS in PD patients. The adverse gastrointestinal factors made impossible the prescription of higher doses of cinacalcet and an eventual benefit of this therapy at higher doses in HS was impossible to evaluate. It is necessary to develop new forms of cinacalcet presentation, in order to avoid GI adverse factors and to improve therapeutic adherence.