What is the basis for thiazide use in treatment of DI? Do thiazide indeed induce water reabsorption in inner medullary segment, as some have reported? Or, is there something else to it?
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Step I thiazide in DI
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this is a very confusing concept
this is wat i found out
thiazide diuretics cause some amt of salt depletion
this in turn causes the extracellular volume to contract which causes a decrease in GFR
this decrease in GFR causes an increase in reabsorption of isotonic solution in the proximal tubule hence decreasing the delivery of fluid to the collecting duct
this is wat i found out
thiazide diuretics cause some amt of salt depletion
this in turn causes the extracellular volume to contract which causes a decrease in GFR
this decrease in GFR causes an increase in reabsorption of isotonic solution in the proximal tubule hence decreasing the delivery of fluid to the collecting duct
Activates RAAS system -> increases Na reabsorption -> water follows sodium
There are 2 contributions.
1, resistance to ADH signaling in nephrogenic DI is not necessarily absolute. On a thiazide, tubular fluid delivered to the collecting duct with a thiazide is at a higher osmolarity, so the residual CD water reabsorption will be a little larger.
Posters above have described the other mechanism. There are 2 factors that contribute to urine excretion... how much is filtered and how much ends up being reabsorbed.
Thiazides decrease water reabsorption by blocking NaCl reabsorption. They also decrease plasma filtration. If you take a normovolemic person and put them on thiazides, they will come to a new steady-state volume below what it was before. This increases sympathetic tone and decreases the amount of plasma filtered in the renal cortex (prox tub receives alpha2 input + more renin).
There are two competing influences... thiazides decrease both reabsorption and filtration. There is no a priori way to guess whether total urine volume will be larger or smaller, but it is observed that patients with nephrogenic DI, the smaller amount of filtration is the dominant effect.
1, resistance to ADH signaling in nephrogenic DI is not necessarily absolute. On a thiazide, tubular fluid delivered to the collecting duct with a thiazide is at a higher osmolarity, so the residual CD water reabsorption will be a little larger.
Posters above have described the other mechanism. There are 2 factors that contribute to urine excretion... how much is filtered and how much ends up being reabsorbed.
Thiazides decrease water reabsorption by blocking NaCl reabsorption. They also decrease plasma filtration. If you take a normovolemic person and put them on thiazides, they will come to a new steady-state volume below what it was before. This increases sympathetic tone and decreases the amount of plasma filtered in the renal cortex (prox tub receives alpha2 input + more renin).
There are two competing influences... thiazides decrease both reabsorption and filtration. There is no a priori way to guess whether total urine volume will be larger or smaller, but it is observed that patients with nephrogenic DI, the smaller amount of filtration is the dominant effect.
As others have stated them, you're not using them to diurese, you're tricking the body into trying to conserve sodium earlier in the nephron. More sodium observed in the more proximal portions, more water follows, and less solute is delivered to the collecting duct, thus less importance of ADH.
Costanzo and Goodman and Gilman explicitly refer to thiazide treatment as for nephrogenic DI and do not mention it as a treatment for central DI... this is probably because no one would give thiazides to a CDI patient when synthetic vasopressin is available.
If the first mechanism I stated does in fact contribute to the efficacy of thiazide diuretics in NDI, it would follow that they are not as helpful in CDI since there is absolutely no insertion of aquaporin channels in the absence of ADH.
If the first mechanism I stated does in fact contribute to the efficacy of thiazide diuretics in NDI, it would follow that they are not as helpful in CDI since there is absolutely no insertion of aquaporin channels in the absence of ADH.
CDI - lack of ADH production/secretion from pituitary. tx - DDAVP
NDI - renal resistance to ADH (various mechanisms) tx - thiazide diuretics
