AIM: Metallic phosphate binders require acidity to dissociate to the free metallic ion and bind phosphorus. Altered gastric acidity may, therefore, influence phosphate-binding efficacy. We evaluated the clinical effect of pantoprazole on the efficacy of calcium carbonate phosphate binders in haemodialysis patients. METHODS: The study had two parts: a cross-sectional study (n = 67), and an interventional, crossover, double-blind, randomized, placebo-controlled trial in 26 patients given pantoprazole 40 mg daily or placebo for two consecutive 6-week periods. RESULTS: The cross-sectional study showed no difference between those on and off acid suppressants in phosphate (1.43 ± 0.45 vs 1.46 ± 0.31 mmol/L, P = 0.782) or other parameters except age (72.2 ± 9.8 vs 63.8 ± 14.8 years, P = 0.01). In the interventional study, phosphate was higher during pantoprazole than placebo (1.59 ± 0.3 vs 1.42 ± 0.3 mmol/L, P = 0.005). Serum calcium (2.37 ± 0.2 vs 2.46 ± 0.2 mmol/L, P = 0.012) and ionized calcium (1.17 ± 0.1 vs 1.22 ± 0.1 mmol/L, P = 0.013) were lower during pantoprazole treatment. CaxPO(4) (3.76 ± 0.7 vs 3.48 ± 0.7 mmol(2) /L(2) , P = 0.032) and intact parathyroid hormone (31.9 ± 21.4 vs 23.6 ± 17.7 pmol/L, P = 0.004) were higher on pantoprazole. CONCLUSION: These results demonstrate clinical evidence for an adverse effect of gastric acid suppression on the effectiveness of calcium carbonate phosphate binders. Given their frequent co-prescription, this interaction may be a minor but common reason why some patients fail to control hyperphosphataemia. Clinicians should regularly assess the need for acid suppressants. Further studies are needed to investigate interactions with other phosphate binders.
RCT Entities:
AIM: Metallic phosphate binders require acidity to dissociate to the free metallic ion and bind phosphorus. Altered gastric acidity may, therefore, influence phosphate-binding efficacy. We evaluated the clinical effect of pantoprazole on the efficacy of calcium carbonate phosphate binders in haemodialysis patients. METHODS: The study had two parts: a cross-sectional study (n = 67), and an interventional, crossover, double-blind, randomized, placebo-controlled trial in 26 patients given pantoprazole 40 mg daily or placebo for two consecutive 6-week periods. RESULTS: The cross-sectional study showed no difference between those on and off acid suppressants in phosphate (1.43 ± 0.45 vs 1.46 ± 0.31 mmol/L, P = 0.782) or other parameters except age (72.2 ± 9.8 vs 63.8 ± 14.8 years, P = 0.01). In the interventional study, phosphate was higher during pantoprazole than placebo (1.59 ± 0.3 vs 1.42 ± 0.3 mmol/L, P = 0.005). Serum calcium (2.37 ± 0.2 vs 2.46 ± 0.2 mmol/L, P = 0.012) and ionizedcalcium (1.17 ± 0.1 vs 1.22 ± 0.1 mmol/L, P = 0.013) were lower during pantoprazole treatment. CaxPO(4) (3.76 ± 0.7 vs 3.48 ± 0.7 mmol(2) /L(2) , P = 0.032) and intact parathyroid hormone (31.9 ± 21.4 vs 23.6 ± 17.7 pmol/L, P = 0.004) were higher on pantoprazole. CONCLUSION: These results demonstrate clinical evidence for an adverse effect of gastric acid suppression on the effectiveness of calcium carbonate phosphate binders. Given their frequent co-prescription, this interaction may be a minor but common reason why some patients fail to control hyperphosphataemia. Clinicians should regularly assess the need for acid suppressants. Further studies are needed to investigate interactions with other phosphate binders.
Authors: Chandan Vangala; Jingbo Niu; Colin R Lenihan; William E Mitch; Sankar D Navaneethan; Wolfgang C Winkelmayer Journal: Clin J Am Soc Nephrol Date: 2018-09-27 Impact factor: 8.237