Hyperkalemia is bananas

Two cases of hyperkalemia in Red clinic this week uncovered a weakness in my own understanding of this issue.  What to do?  Write a blog post, of course.

Potassium balance occurs by moving potassium in and out of cells (thanks to all those pumps that you learned about in medical school) and regulating renal excretion of potassium (more pumps).

Hyperkalemia is due to either too much potassium released from cells or not enough potassium excreted by the kidney.

Cells first
  • Acidosis causes potassium to leave the intracellular space as H+ ions enter
  • Hyperglycemia (DKA), it’s not so much the acidosis in this instance as it is the loss of intracelluar K due to osmotic forces from the hyperglycemia
  • Tissue breakdown- seen most often in tumor lysis syndrome or trauma
To the kidneys
  • Reduced aldosterone secretion: with nl underlying renal function, this is usually a small rise in K.
    • Hyporeninemic hypoaldosteronism
      • RX: NSAIDS, Calcineurin Inhibitors
      • Acute glomerulonephritis
      • Renal insufficiency- most common with diabetic nephropathy
    • RX: Angiotensin system blockers (leads to rise in renin levels)
    • RX: Heparin (usually chronic therapy) can be directly toxic to zona glomerulosa cells
    • Adrenal Insufficiency (only primary AI, the pituitary is not a big regulator of aldosterone)
    • Inherited disorders (that I am conveniently ignoring here)
  • Reduced response to aldosterone
    • RX: Potassium sparing diuretics (spironolactone), trimethoprim (1/2 of Bactrim)
    • Pseudohypoaldosteronism Type 1 (another, albeit well named, congenital disorder that I am ignoring for now)
  • Reduced distal sodium/water delivery (turns off the pumps): anything that decreases effective circulation volume, meaning that dehydration/hypovolemia AND hypervolemia in CHF or cirrhosis can be blamed.
    • Key scenario here is the decompensated CHF patient with poor renal perfusion as they fall off the Starling curve, yet continue their ACE inhibitor and Aldactone.
  • Acute or chronic kidney disease: typically it takes some renal hit (new or ongoing) plus one of the other things above to get truly clinically significant hyperkalemia.  Key scenarios:
    • The fasting dialysis patient.  They are missing the insulin which helps maintain the potassium balance.  This is why we give insulin and glucose  IV when we keep ESRD patients NPO in the hospital.
    • Late stage CKD patients who eat a high potassium diet.  Most patients can eat all the bananas they want and not get hyperkalemia.  Not so if your GFR is 20.
  • Ureterojejunostomy (neobladder). The jejunum (that was used to make the bladder) absorbed potassium in a former life.  Still does.
So how to make the diagnosis?
Think about the etiologies listed above.  What fits for your patient? Look closely at medicines and renal function.
Is this an out of the blue hyperkalemia?  Maybe it’s pseudohypokalemia/lab error- recheck.
If it is an acute rise (that you are pretty sure is real), think moving potassium out of cells.  Tumor lysis syndrome?  DKA?  Acidosis?
If you are still stuck, look to the kidneys. Figure out if aldosterone is working correctly.
  • Check Plasma Renin Activity (PRA), Plasma Aldosterone, and Plasma Cortisol.  Ideally checked after patient is upright for 3 hours (not the time for the 8am cortisol value), or after being given a dose of lasix.
    • Hyporeninemic Hypoaldosteronism- Type 4 RTA will have Low PRA, Low Aldosterone, normal cortisol
      • Usually 50-70 yo diabetic patients with mild/moderate renal insufficiency
    • Primary AI: low aldosterone, low cortisol. Nl or high PRA