Urinary chloride

[loveoforganic2]

Couple questions about importance of urinary chloride in a couple different things.

(1) In Conn syndrome, UW QID 956 lists urinary chloride as being increased, but it should in fact be decreased, correct?

(2) When referring to saline-responsive and saline-resistant metabolic alkalosis, this is more or less contraction alkalosis vs non-contraction alkalosis, correct?

(3) If you have a patient that comes in with metabolic alkalosis, is the interpretation of urinary chloride lead to a DDx that looks like
(a) High - Diuretic misuse
(b) Low - Contraction alkalosis, Primary hyperaldosteronism

Should anything be added to those categories?

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[wanderer]

Couple questions about importance of urinary chloride in a couple different things.

(1) In Conn syndrome, UW QID 956 lists urinary chloride as being increased, but it should in fact be decreased, correct?

(2) When referring to saline-responsive and saline-resistant metabolic alkalosis, this is more or less contraction alkalosis vs non-contraction alkalosis, correct?

(3) If you have a patient that comes in with metabolic alkalosis, is the interpretation of urinary chloride lead to a DDx that looks like
(a) High - Diuretic misuse
(b) Low - Contraction alkalosis, Primary hyperaldosteronism

Should anything be added to those categories?

Vomiting should be category b as well.

 

[MrBeauregard]

Primary hyperaldosteronism absolutely has elevated urine chloride levels. The common causes of saline-resistant metabolic alkalosis are primary hyperaldosteronism, Cushing's disease/syndrome, Bartter and/or Gitelman's syndrome, etc.

 

[loveoforganic2]

Vomiting should be category b as well.

Right you are, thanks

Primary hyperaldosteronism absolutely has elevated urine chloride levels. The common causes of saline-resistant metabolic alkalosis are primary hyperaldosteronism, Cushing's disease/syndrome, Bartter and/or Gitelman's syndrome, etc.

Thanks for the input - couple questions. My assumption was that chloride would follow sodium resorption in primary hyperaldosteronism - why are urinary levels elevated? For Bartter/Gitelman, I assume they're termed saline-resistant just in that metabolic alkalosis will quickly return (it seems like volume repletion would temporarily correct the alkalosis)

 

[alicealicealice]

I understand that Urine chloride is important diagnostically in distinguishing "saline resistant" vs "saline responsive" metabolic alkalosis. Does anyone have an intuitive way for understanding why? Is it that when urinary chloride is high there is something intrinsically wrong with the kidney that it is (1) either wasting Na+ and then Cl- is following or (2) it is reabsorbing Na+ in the collecting ducts which are impermeable to chloride (not sure if thats even true)? Thanks in advance.