PDF OnlyInhibition of calbindin D28K expression by cyclosporin A in rat kidney the possible pathogenesis of cyclosporin A-induced hypercalciuria.Yang, C W; Kim, J; Kim, Y H; Cha, J H; Mim, S Y; Kim, Y O; Shin, Y S; Kim, Y S; Bang, B K Author Information Department of Internal Medicine, Kangnam St. Mary's Hospital, Catholic University Medical College of Korea, Seoul. Journal of the American Society of Nephrology : JASN 9(8):p 1416-1426, August 1998. | DOI: 10.1681/ASN.V981416 Free Metrics Abstract A recent study by Steiner et al. (Biochem Pharmacol 51: 253-258, 1996) demonstrated a decreased calbindin D28K expression in the kidneys of cyclosporin A (CsA)-treated rats. To evaluate the association of renal calcium handling with calbindin D28K expression in CsA-treated rats, two separate experiments (vehicle [VH] versus CsA groups, 1,25-dihydroxyvitamin D3 [VitD] versus VitD + CsA groups) were done simultaneously. CsA (25 mg/kg per d, subcutaneously) and VitD (0.5 microg/kg per d, subcutaneously) were given for 7 d. The CsA group showed decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VH group. The VitD + CsA treatment decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VitD alone. CsA treatment did not affect the serum parathyroid hormone and VitD levels. This study demonstrates an association of calbindin D28K expression with the urinary calcium excretion in CsA-treated rats, and suggests that decreased calbindin D28K expression may play a role in renal calcium wasting. Copyright © 1998 The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved.