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lüll Deletion of the Cl-/HCO3- exchanger pendrin downregulates calcium-absorbing proteins in the kidney and causes calcium wasting Barone S; Amlal H; Xu J; Soleimani MNephrol Dial Transplant 2012[Apr]; 27 (4): 1368-79BACKGROUND: The epithelial calcium channel (ECaC) (TRPV5) and the Cl-/HCO3- exchanger pendrin (SLC26A4) are expressed on the apical membrane of tubular cells in the distal nephron and play essential roles in calcium re-absorption and bicarbonate secretion, respectively, in the kidney. METHODS: A combination of functional and molecular biology techniques were employed to examine the role of pendrin deletion in calcium excretion. RESULTS: Here, we demonstrate that deletion of pendrin causes acidic urine [urine pH 4.9 in knockout (KO) versus 5.9 in wild-type (WT) mice, P<0.03)] and downregulates the calcium-absorbing molecules ECaC and Na/Ca exchanger in the kidney, as shown by northern hybridization, immunoblot analysis and/or immunofluorescent labeling. These changes were associated with a approximately 100% increase in 24-h urine calcium excretion in pendrin null mice. Subjecting the pendrin WT and KO mice to oral bicarbonate loading for 12 days increased the urine pH to approximately 8 in both genotypes, normalized the expression of ECaC and Na/Ca exchanger and reduced the urine calcium excretion in pendrin-null mice to levels comparable to WT mice. CONCLUSIONS: We suggest that pendrin dysfunction should be suspected and investigated in humans with an otherwise unexplained acidic urine and hypercalciuria.|Absorption[MESH]|Animals[MESH]|Anion Transport Proteins/*physiology[MESH]|Bicarbonates/metabolism[MESH]|Blotting, Northern[MESH]|Blotting, Western[MESH]|Calcium Channels/*metabolism[MESH]|Calcium/*urine[MESH]|Chloride-Bicarbonate Antiporters/*metabolism[MESH]|Down-Regulation[MESH]|Fluorescent Antibody Technique[MESH]|Hydrogen-Ion Concentration[MESH]|Kidney/cytology/*metabolism[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Sodium-Calcium Exchanger/*metabolism[MESH]|Sulfate Transporters[MESH]|TRPV Cation Channels/*metabolism[MESH] |