To confirm the inhibitory effect of etidronate on the progression of vascular calcification (VC), 21 patients were randomly enrolled. All 21 patients had end-stage renal disease and were undergoing hemodialysis (HD) three times per week. Patients were observed clinically for 12 months before etidronate treatment and then etidronate was given orally just prior to sleep on the days of dialysis for 23 months. The aortic calcification area (ACA) increased significantly during the 12 months before etidronate treatment. While the ACA of the drug-treated group did not change 12 and 23 months after the initiation of etidronate treatment, the ACA in the control group was significantly elevated 23 months later. These results strongly indicate that etidronate inhibits the progression of VC. Bone mineral density did not change during etidronate treatment. Our findings suggest that etidronate might effectively protect against progressive VC in HD patients.
The present study was designed to determine if etidronate inhibits the development of aortic calcification in hemodialysis (HD) patients. Eighteen Japanese HD patients were divided randomly into etidronate-treated or control groups. Etidronate was given orally at the dose of 200 mg just before sleep on the day of dialysis, which was performed three times per week. In the control group, the aortic calcification area (ACA) increased after 6 months. In the patients who received etidronate, however, when compared to the control group, increases in ACA were significantly suppressed. Serum Ca, P, and the Ca x P product did not change during etidronate treatment. These results suggest that etidronate inhibits the progression of vascular calcification without changes in serum Ca and P levels.
Abstract. The present study was undertaken to determine the effects of etidronate (ED) on calcitriol-induced aortic calcification and bone metabolism in rats with renal failure. Severe aortic calcification was induced by treatment with calcitriol for 3 weeks in rats in which 5 / 6 of the kidneys were removed (SNx group). Treatment of ED (10 mg / kg) together with calcitriol after subtotal nephrectomy (SNx) significantly inhibited thoracic and abdominal aortic calcification 3 weeks after the operation; however, ED (2 mg / kg) was ineffective. The serum levels of osteocalcin and pyridinoline decreased in ED (10 mg / kg) treated-renal failure rats compared with SNx rats. Total bone mineral density (BMD) in the SNx group was lower than that in the sham group, in which animals were treated with calcitriol after a sham operation. The total BMD value in the ED (10 mg/ kg)-treated group was similar to that in the SNx group, whereas the levels of cancellous BMD were low in the ED (10 mg / kg)-treated rats. Our data show that ED at a dosage that suppresses bone metabolism markedly inhibits vascular calcification in rats with renal failure.
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