I don't undersand the mechanism of how Hydrochlorothiazide is used to treat nephrogenic diabetes insipidus. I understand that it works at the early distal convoluted tubule and inhibits the NaCl absorption thereby inc the osmolarity of the urine. But so what? The distal tubule is impermeable to water and so is the collecting tubule in the absence of ADH. Now, since this is nephrogenic DI, there is ADH present but the collecting tubule does not have the receptors for it. So you are still losing water like you used to, it's just a little more concentrated. So it is that some tubules do have receptors and it is those tubules that inc water absorption when a thiazide is used?