achilles
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the treatment for nephrogenic diabetes insipidus is hydroclorthiazide or amiloride. could someone pls explain to me the mechanism of how the diuretics are helpful in Rxing NDI...diuretics result in loss of more water from the body.
i know this is the answer but cannot understand the mechanism. could someone pls help me in understanding this. thanks.
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| Rasul
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Amiloride-for nephrogenic Diabetes insipidus caused by Li- blocks Li uptake in distal tubules and collecting ducts.
Thiazide- I don't understand it clearly too-blocks Na+ rebsorption in distal tubule, creates more isotonic pre-urine.
Na+concentration in renal pasma falls, as a result GFR falls.
Before it get's down to collecting ducts, the isoosmotic sodium chloride from glomerular filtrate gets reabsorbed, with additional free water following along.
So, finite result-urine obtains higher concentration, has less volume.
I know...kinda foggy...did my best...
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| amygdalaa
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hydrochlorothiazides cause na loss in the DCT. This leads to reflex increase in water reabsorption in the PCT. Thus the increase in tonicity of urine.
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| achilles
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thanks very much rasul, amygdalaa...its more clear now.
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| ruhighazi
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Thiazide diuretics in combination with a low salt diet can diminish the degree of polyuria in patients with persistent and symptomatic nephrogenic DI. The potassium-sparing diuretic amiloride also may be helpful, both by its additive effect with the thiazide diuretic and, with reversible lithium-induced disease, by allowing the lithium to be continued.
A thiazide diuretic (such as hydrochlorothiazide, 25 mg once or twice daily) acts by inducing mild volume depletion. As little as a 1 to 1.5 kg weight loss can reduce the urine output by more than 50 percent, from 10 L/day to below 3.5 L/day in one study of patients with nephrogenic DI. This effect is presumably mediated by a hypovolemia-induced increase in proximal sodium and water reabsorption, thereby diminishing water delivery to the ADH-sensitive sites in the collecting tubules and reducing the urine output.
The initial natriuresis and therefore the antipolyuric response can be enhanced by combination therapy with amiloride (or other potassium-sparing diuretic). This regimen has an additional benefit, since amiloride partially blocks the potassium wasting induced by the thiazide.
A loop diuretic, although also capable of inducing mild volume depletion, is not as likely to lower the urine output in DI. These agents decrease sodium chloride reabsorption in the medullary thick ascending limb of the loop of Henle, thereby decreasing the accumulation of NaCl in the medullary interstitium that is essential for the production of a concentrated urine. Thus, a loop diuretic induces relative ADH resistance, an effect that is counterproductive in DI.
The efficacy of amiloride in patients with reversible lithium nephrotoxicity is directly related to its site and mechanism of action. This drug closes the sodium channels in the luminal membrane of the collecting tubule cells. These channels constitute the mechanism by which filtered lithium normally enters these cells and then interferes with their response to ADH.
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| achilles
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wonderful ! thanks ruhighazi !
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