• 作者：Pilar Segura Torres ; ^{pilarnefro@wanadoo.es} ; Francisco J. Borrego Utiel ; M. Carmen Sá ; nchez Perales ; M. José ; Garcí ; a Corté ; s ; M. Mar Biechy Baldá ; n ; Vicente Pé ; rez Bañ ; asco
• 关键词：Cinacalcet ; Hemodiá ; lisis ; Hiperparatiroidismo secundario ; Paricalcitol ; Sevelamer
• 刊名：Di¨¢lisis y Trasplante
• 出版年：2010
• 出版时间：April-June 2010
• 年：2010
• 卷：31
• 期：2
• 页码：37-41
• 全文大小：179 K

Background

Several authors have shown the difficulty of achieving the targets established in published guidelines for the treatment of secondary hyperparathyroidism. Cinacalcet can reduce serum parathyroid hormone (PTHi) levels, thus helping to achieve established targets. The aim of the present study was to analyze how cinacalcet can facilitate control of secondary hyperparathyroidism by comparing our results with the target levels recommended in guidelines and to identify the factors that could influence response to this drug.

Material and methods

We retrospectively collected information on the response of 74 hemodialysis patients with secondary hyperparathyroidism (baseline PTHi levels >300 pg/ml) who were treated with cinacalcet for at least 6 months. We recorded serum calcium (Ca), phosphorus (P), and PTHi levels at 3, 6, 9 months and at the end of follow-up. The baseline and final doses of phosphorus captors were also recorded.

Results

At the end of the follow-up, cinacalcet reduced serum levels of PTHi by 36 % , P by 13.2 % , Ca by 6 % , and calcium-phosphorus product (CaxP) by 12.9 % . At the start of treatment, P was >5.5 mg/dl in 38.4 % of the patients, Ca was <8.4 mg/dl in 2.7 % , and CaxP was >55 mg²/dl² in 37.8 % . After cinacalcet treatment, 50 % of patients had PTHi <300 pg/ml, the percentage of patients with P >5.5 mg/dl was reduced to 24.7 % , the prevalence of hypocalcemia increased to 12.2 % , and the percentage of patients with CaxP>55 mg²/dl² was reduced to 14.9 % . The presence of hypocalcemia was independent of baseline PTHi levels and the degree of control of hyperparathyroidism reached after cinacalcet treatment. Most patients were managed without vitamin D (paricalcitol), which was discontinued in 24.3 % who received this drug before cinacalcet therapy and was added to treatment in only 13.5 % of patients with inadequate control of PTHi. After cinacalcet treatment, calcium carbonate doses increased (baseline 1.5¡À3.8 g/day vs final 2.4¡À4.9 g/day; p=0.03) with a non-significant reduction in sevelamer doses.

When we analyzed the degree of final response to cinacalcet, we observed that levels of PTHi at 3 months were significantly lower in patients who reached PTHi <300 pg/ml at the end of follow-up, with lower final doses of cinacalcet (78 % of patients with doses of 30 mg/day or less). When we reviewed the effect of phosphorus captors, we found that patients with higher doses of sevelamer at baseline showed a worse response, required higher cinacalcet doses, and less frequently achieved target PTHi levels. Multiple regression analysis confirmed that the degree of response depended on baseline PTHi levels and baseline sevelamer doses.

Conclusions

Cinacalcet facilitates control of secondary hyperparathyroidism. The PTH levels reached after 3 months of cinacalcet treatment have a prognostic value in predicting final response. The degree of response depends on the severity of secondary hyperparathyroidism, reflected by baseline PTHi levels and the sevelamer doses prescribed.