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Excessive taurinuria occurs in vitamin D deficiency as a component of the generalized aminoaciduria of that state. Aminoaciduria was originally ascribed to hyperparathyroidism (increased PTH) in vitamin D-deficiency rickets, especially because aminoaciduria and the increase in PTH disappear after vitamin D repletion. Dabbagh showed that (1) increased taurinuria was due to a defect in the proximal tubule brush border membrane; (2) The Vmax of taurine uptake into brush border membrane vesicles was reduced, possibly related to a paucity of the TauT transporter in the membrane; (3) Animals with low PTH and vitamin D deficiency still had taurinuria and decreased taurine uptake; (4) cAMP incubation did not alter BBMV taurine uptake. The observation that vitamin D-deficiency rickets due to a vitamin D receptor (VDR) mutation results in aminoaciduria despite normal or high 25(OH)D and 1,25(OH)2D values suggests a role for the VDR in taurinuria. Han and Chesney have shown a vitamin D response element (VDRE) in the promoter region of the TauT gene which, under conditions of vitamin D deficiency, results in reduced transcription and reduced TauT protein in LLC-PK1 cells. Thus, in vitamin D deficiency, lower VDRE activation results in lower levels of taurine uptake by tubule cells (or vesicles) and taurinuria. Repletion of 1,25(OH)2D restores TauT transporter activity and taurinuria abates. |
