Recent findings by Nijenhuis et al50 indicate that enhanced passive Ca2+ transport in the proximal tubule due to extracellular volume contraction may be responsible for the hypocalciuria that develops during chronic thiazide treatment, while specifically reduced renal expression levels of the epithelial transient receptor potential Mg2+(–ion) channel (TRPM6) were found in their mouse models apparently responsible for inappropriately high fractional Mg2+ excretion into the urine. This evidence concerns the gene TRPM6 and Hypocalciuria.