raves
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i read somewhere that chronic use of thiazides leads to a fall in GFR n so would be beneficial in DI??
any comments please
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| study_ing
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this is kinda confusing but i'll try
in DI the site where water reabsorption is not taking place will be the Collecting duct, ight, that is the site of AXN of ADH.
by givinng diuretics, u relatively dehydrate the pt so that absorption occurs proximally
i dont have a source or a tXt book refernce for the explanation so its not a 100% reliable one
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| raves
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but not having ADH is kinda being on diuretics,he still can reabsorb water from proximal tubule study_ing(which is indeed the site of maximal water reabsorption) but this is about GFR!!
but thanks for paying attention n trying buddy.
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| study_ing
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i agree.. even the guty who tot us warned us about that!!
but hey ..its medicine!!
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| tolito
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here is a reference for you
http://jasn.asnjournals.org/cgi/content/full/15/1...
Thiazide diuretics inhibit the NaCl co-transporter (NCC/TSC) in the renal distal convoluted tubule (DCT). The DCT is water impermeable and considered to be part of the diluting segment. Therefore, the water-preserving effect of thiazides is unlikely related to a direct effect on the DCT. In fact, the most widely accepted hypothesis suggests that the antidiuretic action of thiazides is secondary to increased renal sodium excretion. The renal sodium loss causes extracellular volume contraction leading to lowered GFR and increased proximal tubular sodium and water reabsorption. Hence, less water and solutes are delivered to the distal tubule and collecting duct and are lost as urine
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| raves
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 thanks tolito nice.
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