Euvolemic hypernatremia

[alex78112]

Hi everyone,

I'm having a hard time understanding this notion:
In patients with diabetes inspidus, there is a loss in free water, which results in hypernatremia (that, I can understand).
However, why is the urinary sodium excretion also high?
In my understanding, if there is a loss in free water, the body would compensate by increasing aldosterone secretion and reducing ANP secretion => less sodium excretion => more sodium reabsorption, water follows => euvolemic hypernatremia.
But this doesn't seem to be the case as sodium urinary excretion stays high... Why is that?

Thanks for your help 🙂

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[mk04447]

Look at the treatment for the answer. Give ADH, not aldosterone. Salt resorption has a transport maximum. Understand?

 

[alex78112]

Not really. I understand that salt resorption has a transport maximum however it is not reabsorbed whatsoever in diabetes insipidus since there is high natriuresis... 🙁

 

[Ven0m]

However, why is the urinary sodium excretion also high?

Is the sodium excretion high? Everything I've read says in both central + nephrogenic DI, urine volumes are excessive + dilute.

edit: maybe they're talking about the triphasic response after you section the pituitary stalk:
- The first phase is characterized by very low ADH and thus very large urine output that's dilute. This is diabetes insipidus.
- The second phase is characterized by very high ADH because by this time, the posterior pituitary axons containing the ADH have begun lysing and are now releasing huge amounts of ADH into circulation (basically, this is no longer diabetes insipidus, but SIADH). This obviously increases urine sodium concentration excessively.
- The third phase is characterized by a very low ADH again because all the ADH has been used up. So urine volume is excessive and dilute again (diabetes insipidus has returned).

from kaplan physiology 2016 p. 274

 

[STEPinthenameoflove2018]

Hi everyone,

I'm having a hard time understanding this notion:
In patients with diabetes inspidus, there is a loss in free water, which results in hypernatremia (that, I can understand).
However, why is the urinary sodium excretion also high?
In my understanding, if there is a loss in free water, the body would compensate by increasing aldosterone secretion and reducing ANP secretion => less sodium excretion => more sodium reabsorption, water follows => euvolemic hypernatremia.
But this doesn't seem to be the case as sodium urinary excretion stays high... Why is that?

Thanks for your help 🙂

Losing free water alone in DI doesn’t activate the RAAS system so there wouldn’t be an increase in aldosterone.

Not sure what you mean by high sodium excretion. Relative to what? What source are you reading from that might help with the context - also I’m assuming you’re talking about nephrogenic DI - this can be caused by a variety of different things (ex hypercalcemia ... that would block sodium reabsorption and cause an increase in sodium excretion...)

Hopefully this isn’t on STEP lol





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