Thiazides leading to Lithium toxicity

[str8flexed]

UW says: Thiazides volume deplete you, so the prox tubule wants to reabsorb more Na+, and Lithium is reabsorbed with Na+ so the low therapeutic index of Lithium allows it to be easily OD'd.

I have some questions:

Would ANY diuretic that volume depletes you cause the same effect? Furosemide is a stronger diuretic. Do the other diuretics have the same effect?

Thiazides act on the distal tubule, after the macula densa at the junction of the ascending limb of Henle and the distal convoluted tubule. Does the kidney just "know" you're volume depleted?

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[a winner is you]

Yes, to all of the above. The only thing I think you're wrong about is that Li+ is not absorbed "with" Na+, it's absorbed in place of Na+, your kidney doesn't differentiate the cations well.

 

[SomeDoc]

UW says: Thiazides volume deplete you, so the prox tubule wants to reabsorb more Na+, and Lithium is reabsorbed with Na+ so the low therapeutic index of Lithium allows it to be easily OD'd.

I have some questions:

Would ANY diuretic that volume depletes you cause the same effect? Furosemide is a stronger diuretic. Do the other diuretics have the same effect?

Thiazides act on the distal tubule, after the macula densa at the junction of the ascending limb of Henle and the distal convoluted tubule. Does the kidney just "know" you're volume depleted?

NSAID's will have the same effect as well, leading to Li+ toxicity via an increased Na+ reabsorption mechanism, with Li+ reabsorbed as an Na+ analogue.

 

[str8flexed]

NSAID's will have the same effect as well, leading to Li+ toxicity via an increased Na+ reabsorption mechanism, with Li+ reabsorbed as an Na+ analogue.

Yes, because NSAIDS reduce prostaglandin synthesis; prostaglandins normally dilate afferent arterioles. Constricting afferent arterioles decreases GFR that results in tricking the kidney into thinking that the body is volume depleted, and therefore want to reabsorb Na+/Li+...