Thread by @kidney_boy

This is not a good definition of SIADH.

Samad, Navira, and Ian Fraser. 2017. “Severe Symptomatic Hyponatremia Associated with the Use of Polyethylene Glycol-Based Bowel Preparation.” Endocrinology, Diabetes & Metabolism Case Reports. doi.org/10.1530/edm-16….

Ref 8 in 2nd pic.

ADH is "fails to be suppressed despite the sodium falling below osmotic threshold for ADH release" in lots of conditions that are not SIADH: CHF, cirrhosis, volume depletion to name some of the headliners.

Almost all causes of hyponatremia are driven by non-osmotic ADH release:
1. non-physiologic (SIADH) or
2. due to poor perfusion with increased volume (CHF, cirrhosis, nephrotic sx) or
3. due to poor perfusion with decreased volume (volume depletion, thiazide)

Note that the physiology of numbers 2 and 3 are identical, physiologic release of ADH due to poor perfusion, despite patients that clinically look wildly different.

ADH in this situation physiologically "makes sense" because ADH binds to V1 receptors in the vasculature, causes vasoconstriction which can improve perfusion. Here the body is sacrificing a normal osmolality in the name of perfusion. Fair choice.

The proper definition of SIADH is the release of ADH where perfusion is normal and the osmolality is low. When the body is in this situation, there is no physiologic benefit of the ADH. The body is sacrificing a normal osmoregulation with no need to improve perfusion.

The few cases of hyponatremia that are ADH-independent are:
• Tea & Toast
• Beer drinkers potomania
• Psychogenic polydipsia
• Oliguric kidney failure