Potassium Handling by the Kidney

Lecture given:


Describe the pathophysiology of potassium disorders

  • Normal ECF [K] = 3.5-5 mmol/L
  • Normal ICF [K] = 150 mmol/L
  • Crucial for generating cell membrane potential
Eventually extreme hyperkalemia will end up in sine wave, and patient will die!
  • K regulation done through CCD (cortical collecting duct) principal cells, under the influence of aldosterone
    • Both RAAS and high ECF [K] are triggers to increase aldosterone activity
  • The gut can excrete K in extreme kidney dysfunction, or through massive diarrhea
  • Other factors influencing K handling include:
    • ADH (increase K secretion)
    • Increased urine flow (maintain K gradient past the principal cells)
    • inadequate urinary Na (nothing to push K out of the principal cells)
    • Alkalosis (less H to secrete by alpha-interacalated cells, more need for K secretion)
  • Disorders of K arises when 2 out of 3 mechanisms are not working:
    • Intake - diet, tissue necrosis, massive hemolysis releasing ICF K into ECF
    • Output - Mostly through kidneys in response to aldosterone, some from GI (too much excretion can be caused by GI or kidney, not enough excretion is only the kidney's problem)
    • Shift - Insulin, beta receptors, Na/K/ATPase (digoxin blocks this), rare diseases (familial periodic paralysis), rapid cell expansion (B12 for pernicious anemia)
  • Transtubular potassium gradient (TTKG)
  • If TTKG >7: aldosterone is present and working, can generate a high gradient
    • If ingesting K, urine K should increase, generating a high TTKG. If it's not the case, then aldosterone is not working
  • If TTKG <2: aldosterone absent/blocked, or inadequate urine Na and flow. Cannot generate high gradient

Provide the differential diagnosis of hypo- and hyperkalemia & describe the appropriate management of hypo- and hyperkalemia


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