Liddle syndrome metabolic alkalosis

[DoctorG2020]

Does anyone know the physiologic mechanism behind the metabolic alkalosis in Liddle syndrome? For the majority of the other renal tubular defects, the alkalosis is caused by an increase in aldosterone due to volume loss. For this particular syndrome, there is no aldosterone increase, and I'm wondering if I'm missing something simple! Thanks!

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[68PGunner]

ENaC overactivity results in absorption of sodium and loss of potassium through ROMK on the principle cell. You now have hypokalemia.

Body will try to compensate the hypokalemic state through the alpha intercalated cells through H+/K+ exchanger ATPase, leading to excretion of H+, and thereby giving you a metabolic alkalosis state.

 

[Foot Fetish]

ENaC overactivity results in absorption of sodium and loss of potassium through ROMK on the principle cell. You now have hypokalemia.

Body will try to compensate the hypokalemic state through the alpha intercalated cells through H+/K+ exchanger ATPase, leading to excretion of H+, and thereby giving you a metabolic alkalosis state.

This question is mere child's play for @68PGunner

 

[donovank730]

think about liddle syndrome as hyperaldosteronism without actual elevated aldosterone. It will have all the same metabolic findings, and produce the same hormonal negative feedback (decreased renin)

As said before it works through ENaC, which is the same location as aldosterone

It's good to lump SAME(syndrome of apparent mineralocorticoid excess) with liddle, because it has the same exact profile, but the mechanism is different(cortisol binding aldosterone receptors in the collecting duct)