Potassium homeostasis

Potassium

Potassium Space is Huge

• NaK ATPase constantly bailing Na to keep K inside
• K "bath" used to stop hearts for surgery
• diarrhea loss can be much higher than nl (up to 100 mEq/day)
• creates metabolic acidosis with hypokalemia  (in most cases acidosis comes with hyperkalemia)

K homeostasis

• rhabdomyolysis may cause dangerous hyperkalemia

Physiology of K homeostasis

Death by avocado  -  response to K intake

alpha intercalated cells and principal cells fine tune the 13% of K+ that remains in the tubule after reabsoption by the proximal convoluted tubule and thick ascending limb of the loop of Henle.  alpha cells reabsorb K+ if there is hypokalemia.  principal cells secrete K+ if there is hyperkalemia.  Also, the principal cells are the target of the adrenal medulla hormone, aldosterone, which increases Na+ reabsorption and K+ excretion.

There appears to be a well-developed system for sensing potassium by the pancreas and adrenal glands. High potassium states stimulate cellular uptake via insulin-mediated stimulation of sodium-pump activity in muscle and stimulate potassium secretion by the kidney via aldosterone-mediated enhancement of distal renal expression of secretory potassium channels (ROMK).

Low potassium states result in insulin resistance, impairing potassium uptake into muscle cells, and cause decreased aldosterone release, lessening renal potassium excretion. This system results in rapid adjustments in immediate potassium disposal and helps to provide long-term potassium homeostasis.

Na and K levels Interact  --  Edelman equation

Plasma [Na +] = Na+ + K+/TBW

Kidneys reabsorb all filtered load of K (720 mEq/day) - most in collecting duct (principal cells)

Bartter's Syndrome  - thick ascending limb  = same effect as loop diuretics

Gittleman Syndrome - DCT - resembles thiazide diuretic

Potassium sparing diuretics

• amiloride - Naa channel blocker
• reduced aldosterone (ACE inhibitors) or aldosterone receptor blockers (spinolactone)