title: Low calcium (1.25 mmol/L) dialysate can normalize relative hypoparathyroidism in CAPD patients with low bone turnover.
abstract: Recently, several reports have suggested that there is a higher incidence of low turnover bone in the absence of aluminium exposure in peritoneal dialysis patients than in hemodialysis patients. Relative hypoparathyroidism with mild hypercalcemia, induced by a positive calcium balance, is considered to be one of the major causes of this disorder. Thus, we recruited 9 continuous ambulatory peritoneal dialysis (CAPD) patients with relative hypoparathyroidism and low bone turnover [intact parathyroid hormone (iPTH) < 50 pg/mL, intact osteocalcin < 10.0 ng/mL] who had been prescribed 1.75 mmol/L calcium (Ca) dialysate for 5.0 +/- 0.3 years. They were then treated by low Ca (1.25 mmol/L) dialysate for nine months without vitamin D and aluminum administration. Intact PTH and bone metabolic markers [intact osteocalcin, alkaline phosphatase (ALP)] were measured every three months. Intact PTH levels increased from 21.1 +/- 3.8 to 159.2 +/- 32.8 pg/mL after the first three months; thereafter, those levels were maintained at around 150 pg/mL. On the other hand, intact osteocalcin levels rose consecutively from 6.7 +/- 1.2 to reach 22.0 +/- 3.8 ng/mL after nine months. Interestingly, the pattern of time course changes between PTH and intact osteocalcin was different. ALP activity did not change during the nine-month period. Corrected serum calcium was significantly decreased (p < 0.001) to approximately 0.25 mmol/L within one month, and the level remained almost the same thereafter. The serum phosphate level did not change without adjusting the original dose of calcium carbonate as a phosphate binder. We concluded that low Ca dialysate (1.25 mmol/L) is effective for the treatment of CAPD-related hypoparathyroidism with low bone turnover.
authors.affiliation: Second Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Shigematsu
authors.forename: Y
authors.initials: Y
authors.lastname: Kawaguchi
authors.forename: H
authors.initials: H
authors.lastname: Kubo
authors.forename: M
authors.initials: M
authors.lastname: Nakayama
authors.forename: N
authors.initials: N
authors.lastname: Kato
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: N
authors.initials: N
authors.lastname: Osaka
authors.forename: H
authors.initials: H
authors.lastname: Hayakawa
authors.forename: A
authors.initials: A
authors.lastname: Ogawa
authors.forename: O
authors.initials: O
authors.lastname: Sakai
mesh_terms: D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood; D002118:Calcium / Q000008:administration & dosage*; D002119:Calcium Carbonate / Q000008:administration & dosage; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000503:physiopathology / Q000628:therapy*; D015314:Dialysis Solutions / Q000008:administration & dosage*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006934:Hypercalcemia / Q000503:physiopathology / Q000628:therapy; D007011:Hypoparathyroidism / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010281:Parathyroid Hormone / Q000097:blood; D010531:Peritoneal Dialysis, Continuous Ambulatory; D010710:Phosphates / Q000097:blood
chemical_list: D015314:Dialysis Solutions; D010281:Parathyroid Hormone; D010710:Phosphates; D015675:Osteocalcin; D000469:Alkaline Phosphatase; D002119:Calcium Carbonate; D002118:Calcium