Can someone explain to me why in SIADH typical we aren't worried about hypokalemia

[drjorilla]

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When ever read about SIADH the main focus is hyponatremia, and reduction in BUN and serum osmolarity. I was wondering if someone could explain why reductions in the other electrolytes aren't as concerning. wouldnt every valued be diluted ?

 

[Malyck]

My guess is that the other values are in much smaller concentrations already (i.e. K and Ca) and the only value that would adversely affected to a large degree by dilutional events (hyperglycemia, hyperlipidemia, etc.) would be the electrolyte that would have the highest concentration (Na). This is just a guess though, if anyone has a different answer I'd like to know.

 

[thehundredthone]

Absolutely, Na (and Cl) correlates with ECF due to it's much larger concentration. ICF correlates closer with K, and the loss of K (from ECF) can cause ICF contraction.

 

[hurryupnwait]

You worry about rapid shifts in serum osmol mostly because of its effect on cerebral edema. That being said, serum osm = 2*Na + glc/18 + BUN/2.8. K and Ca are mostly intracellular, and don't have large effects on serum osm (you also expect renal compensation to maintain their levels, while serum Na is more sensitive to volume status). This is also the basis for disequilibrium syndrome with rapidly declining BUN in dialysis patients, and also why reductions in serum ammonia levels don't majorly factor into it.

 

[Phloston]

SIADH is a euvolemic hyponatremia. ADH initially increases volume status through free water reabsorption at the medullary collecting duct. Then it's likely that the PCT decreases NaCl reabsorption after chronically high levels of ADH are present in order to compensate for the augmented volume status. That's why sodium drops in the face of euvolemia.

A secondary element would be that chronically high ADH levels lead to decreased aldosterone levels in order to compensate for volume status, where Na+ is further not reabsorbed, leading to hyponatremia. The reason this is likely not the main mechanism is because we don't see metabolic acidosis or hyperkalemia with SIADH.

The reason we don't see hypokalemia (decreased K+ extracellularly) though is because a reduction in extracellular [K+] secondary to free water retention would be counterbalanced by the shift of K+ from the ICF --> ECF, since it's [ ] is greater in the ICF. But this effect wouldn't happen with Na+ because it's [ ] is greater in the ECF even in the face of SIADH-induced free water retention, so no ICF --> ECF shift can occur to rescue the drop in plasma Na+.