Treatment of secondary hyperparathyroidisms of predialysis chronic renal failure with low doses of 1.25(OH)2D3

• Published in: Nihon Jinzo Gakkai shi Vol. 37; no. 10; pp. 543 - 548
• Main Authors: KATO, Naohiko, KASAI, Kenji, KAWAGUCHI, Yosindo, YAMAMOTO, Hiroyasu, SHIGEMATU, Takashi, SAKAI, Osamu
• Format: Journal Article
• Language: Japanese
• Published: Japan Japanese Society of Nephrology 01-10-1995
• Subjects: 1,25(OH)2D3, predialysis chronic renal failure, secondary hyperparathyroidism, renal function; Aged; Bone Density; Calcitriol - administration & dosage; Calcitriol - blood; Female; Humans; Hyperparathyroidism, Secondary - drug therapy; Kidney Failure, Chronic - complications; Kidney Failure, Chronic - therapy; Male; Middle Aged; Prospective Studies; Renal Dialysis
• ISSN: 0385-2385; 1884-0728
• DOI: 10.14842/jpnjnephrol1959.37.543

Although disorders of renal calcitriol synthesis play an important role in the pathogenesis of secondary hyperparathyroidism in the early and moderate phase of chronic renal failure, the treat ment of secondary hyperparathyroidism with vitamin D metabolite has not attained consensus from the view point that is accelerates the progression of renal disease. The aim of this study was to evaluate the efficacy and adverse effect of low-dose daily oral treatment of 1.25 vitamin D for patients with mild to moderate renal failure. Fifteen chronic renal failure patients with serum creatinine ranging from 2.5 to 6.1 mg/dl and serum intact parathyroid hormone ranging from 100 to 450 pg/ml, were treated with oral 0.25-0.5μ g of 1.25 vitamin D for six months, after a six month control periods. In the six months control periods, serum intact parathyroid hormone, alkaline phosphatase activity, and bone gla protein increased significantly, however after the treatment of 1.25 vitamin D, serum intact parathyroid hormone, alkaline phosphatase activity, and bone gla protein decreased signifi cantly. Serum calcium concentration increased significantly after the initiation of 1.25 vitamin Dtreatment, so it could not be ascertained whether or not 1.25 vitamin D directly suppressed parathyroid hormone synthesis. Bone mineral densities did not change within one year. Renal function was evaluated from the slopes of the reciprocal serum creatinine concentration versus time. The slopes did not change after the administration of 1.25 vitamin D In conclusion, 1.25 vitamin D treatment of secondary hyperparathyroidism in patients with mild to moderate renal failure had beneficial therapeutic effect on humoral bone parameters, and did not show any adverse effect on renal function.