title: Control of parathyroid function in patients with a short history of hemodialysis.
abstract: Secondary hyperparathyroidism (SHPT) is one of the serious complications in patients with chronic kidney disease. Parathyroid glands secrete parathyroid hormone (PTH), stimulated partly by hyperphosphatemia and hypocalcemia complicating chronic kidney disease (CKD). Use of a calcium-based phosphate binder might be sufficient to reduce serum PTH levels in mild SHPT, while the recent K/DOQI clinical guidelines recommended vitamin D therapy for dialysis patients with serum level of intact parathyroid hormone of 300 pg/mL or more. We conducted a 6-month prospective controlled trial of 50 patients initiating hemodialysis therapy who were randomized to receive oral calcium carbonate alone or the drug plus oral vitamin D sterol, calcitriol or alfacalcidol. The primary end point was the proportion of randomized patients who had a mean PTH level of 300 pg/mL or less at the end of this study. The secondary end point included the percent change in the values for corrected calcium, phosphorus, the calcium-phosphorus product, and PTH. Eighty percent of patients receiving calcium carbonate without vitamin D sterols (20 of 25) reached the primary end point-a mean PTH level of 300 pg/mL or less after the period-as compared with 84% of those receiving calcium carbonate and vitamin D sterol (21 of 25) (Mantel-Haenszel odds ratio 0.76, 95% confidence interval: 0.18-3.25, P = 0.71). The other effects of the two regimens on the secondary end points were not significantly different after 6 months. In SHPT of dialysis patients initiating hemodialysis, oral calcium carbonate use alone was not inferior to additional vitamin D sterol use with calcium carbonate in reducing serum PTH levels. Our result indicated that, if serum calcium and phosphorus levels are controlled primarily regardless of used agents, it will be followed by reduction of serum PTH level in these patients.
authors.affiliation: Division of Nephrology and Dialysis Center, Kobe University School of Medicine, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nishi
authors.forename: Takashi
authors.initials: T
authors.lastname: Sato
authors.forename: Toru
authors.initials: T
authors.lastname: Kurihara
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kurosawa
authors.forename: Masafumi
authors.initials: M
authors.lastname: Fukagawa
mesh_terms: D000284:Administration, Oral; D002117:Calcitriol / Q000008:administration & dosage / Q000627:therapeutic use; D002118:Calcium / Q000097:blood; D002119:Calcium Carbonate / Q000008:administration & dosage / Q000627:therapeutic use; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006887:Hydroxycholecalciferols / Q000008:administration & dosage / Q000627:therapeutic use; D006962:Hyperparathyroidism, Secondary / Q000188:drug therapy / Q000517:prevention & control*; D007676:Kidney Failure, Chronic / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D010280:Parathyroid Glands / Q000503:physiopathology*; D010281:Parathyroid Hormone / Q000097:blood*; D010758:Phosphorus / Q000097:blood; D011446:Prospective Studies; D006435:Renal Dialysis; D013997:Time Factors
chemical_list: D006887:Hydroxycholecalciferols; D010281:Parathyroid Hormone; D010758:Phosphorus; D002117:Calcitriol; D002119:Calcium Carbonate; D002118:Calcium; C008088:alfacalcidol