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Hey friends,

as we all know, Thiazide diuretics cause hypercalcemia. then how could we use it in the treatment of Nephrogenic diabetes insipidus? In FA,one of the reasons for NDI is hypercalcemia. it is getting so confusing. please guide. thank you in advance.
 

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Hey friends,

as we all know, Thiazide diuretics cause hypercalcemia. then how could we use it in the treatment of Nephrogenic diabetes insipidus? In FA,one of the reasons for NDI is hypercalcemia. it is getting so confusing. please guide. thank you in advance.
Diabetes insipidus is obviously dumping lots of free water, this leads to hypernatremia or a "hypertonic volume contraction". This volume contraction will naturally activate ATII to constrict both afferent (little effect) but most importantly the efferent arteriole, thus increasing FF. I'll remind you that increasing the FF (which is a protein free ultrafiltrate) will accumulate plasma protein and thus increase capillary hydrostatic pressure. This will result in greater reabsorption of water by the PT. The reason we use thiazides is to decrease the concentration of solute while they body is doing its part taking care of the volume. Yes thiazides normally will dump water and solute, but in this case the body already has a mechanism in place to take care of the volume loss, and with the thiazides we are helping with the solute problem.

About the hypercalcemia deal, Thiazides do cause higher reabsorption of Ca in the DT. The reason why hypercalcemia causes DI is because high plasma Ca inhibits the co-transporter in the ascending part of the loop, so just like a loop diuretic it reduces the medullary interstitial osmolarity thats required for the kidney to respond adequately to ADH. But since ADH doesn't work already, we can do no harm with it.

Hope that makes sense bro, if not i'll try to do a better job for you. [email protected]
 

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Yea,, using thiazides increases excretion of solute in early DCT and Na loss,,hence subsequently increases activation of the RAA system which facilitates increased retention of salt in late DCT nd CT,,this drags along water,,so helps increase both salt nd water retention,,u myte say paradoxically,,,de mechanism of NDI wit hypercalcemia iz as stated above,,nd iz advantageous be coz by decreasing Na reabsorption in LOH,,increases delivery to de distal tubules to facilitate its absorption along wit water,,de most important thing to note iz free water iz being lost eitherwayz in de absence/dysfunction of AVP receptors nd using the thiazides increases to some extent Na and H2O reabsorption,,hope that will do,,
 
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