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Old 03-29-2013
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Drug Thiazides in Nephrogenic Diabetes Insipidus?

who wants to try explain how thiazide diuretics are useful for nephrogenic diabetes insipidus?
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Old 03-29-2013
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So Thiazides act by inhibiting the Na/Cl transporter in the DCT, which leads to sodium, chloride, and water loss. This leads to a decrease in GFR. Consequently, to maintain the GFR, there will be an increase in water and sodium uptake in the PCT. This means that less water and solute will be delivered to the DCT, which leads to less water being lost in the urine. Its kind of a funny action, the Thiazides are sort of acting against themselves...
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Old 03-29-2013
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Quote:
Originally Posted by CisternaChyli View Post
So Thiazides act by inhibiting the Na/Cl transporter in the DCT, which leads to sodium, chloride, and water loss. This leads to a decrease in GFR. Consequently, to maintain the GFR, there will be an increase in water and sodium uptake in the PCT. This means that less water and solute will be delivered to the DCT, which leads to less water being lost in the urine. Its kind of a funny action, the Thiazides are sort of acting against themselves...
basically the same mechanism
as thiazides inhibit NaCl transport and the part of nephron involved is diluting segment (no H2O absorption)
there is no separation of solute from water (water stays coupled with NaCl) and is absorbed with Na in late DCT and cortical collecting ducts by the aldosterone
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Old 03-29-2013
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Default Thiazide and Nephrogenic Diabetes Insipidus

As mentioned already, thiazides by acting in early distal tubule block Na+/Cl- channel and therefore, decrease their movement from tubular lumen back into the cells. Keeping in mind that this segment is almost completely impermeable to water and hence "a diluting" segement, thiazide, therefore results in loss of not just water but also salts(Na+/Cl-). This leads to mainly:

1. Decrease of GFR, resulting into compensatory increase of Proximal tubules activity for Na+/Cl-(along with water) re-absorption which shall decrease their delivery to late distal and collecting tubule and thus causing the decrease need for ADH.

2. Keep in mind the fact that while the thiazide is in play, the cells don't reabsorb salts in distal tubule. This salt along with the property of distal tubule as diluting segment deliver, to distal tubule and colleecting duct, a urine which is not dilute enough(otherwise the primary stimulus for ADH realease) as to require the ADH action. Hence therefore improvement of Nephrogenic Diabetes.

Hope it helps!
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Old 03-30-2013
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Nice explanation here
Treatment for nephrogenic diabetes insipidus?

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