Great question - they lead to mild hypovolemia which activates the RAAS which leads to enhanced sodium and water reabsorption in the PCT which leads to less polyuria. Although it seems paradoxical it does seem to be effective in nephrogenic DI
@NinjaNerdOfficial I had this exact same question too and loved your explanation of it here as well. I have a follow up question to add on to it if that's okay. If the cause of the nephrogenic DI is hypokalemia or hypercalcemia, then I assume you correct the abnormality (and/or underlying cause) and you solve the issue. But in instances of CKD or inheritance, do you keep them on long term thiazide tx? Lifetime?
Salt tablets have no effect in treatment at all, every nephrologist will get a heart attack if you administer them to your patients. Fluid restriction is key to recompensate the normal state of sodium levels in chronic and/or asymptomatic patients if the Na is between 120-135 mmol/l. If acute or symptomatic the i.v. treatment is the way to go but as slowly as possible, max 10 mmol/l per day. Otherwise you risk an irreversible central pontine myelinolysis.
In complications of SIADH: The increase in aquaporin channels increases re-uptake of water from the urine, which leads to dilution of blood, and thereby, hyponatremia. But the increased water retention would lead to decreased aldosterone (to counteract the hypervolemia), which would promote sodium excretion in the urine. Water follows sodium, so more water should go into the urine, but since ADH is increased, it just refuses to let that water go, and continues the pattern. How then, would euvolemia be achieved? @ euvolemic hyponatremia
