(Journal Article): Inhibition of calbindin-D28K expression by cyclosporin A in rat kidney: the possible pathogenesis of cyclosporin A-induced hypercalciuria.
 
Yang CW, Kim J, Kim YH, Cha JH, Mim SY, Kim YO, Shin YS, Kim YS, Bang BK (Department of Internal Medicine, Kangnam St. Mary's Hospital, Catholic University Medical College of Korea, Seoul.)
 
IN: J Am Soc Nephrol 1998; 9:1416-1426
Impact Factor(s) of J Am Soc Nephrol: 6.644 (2004), 7.499 (2003), 6.337 (2001)

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.

TYPE OF PUBLICATION: Original article

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• Thongboonkerd V, Zheng S, McLeish KR, Epstein PN, Klein JB. Proteomic Identification and Immunolocalization of Increased Renal Calbindin-D28k Expression in OVE26 Diabetic Mice. Rev Diabetic Stud 2005. 2: 19-26.
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