Mel from BC asks: Why does “tac” (tacrolimus) cause hyperkalemia? Do other medications in this family also cause hyperkalemia?
My response
“Tac”, or tacrolimus is commonly used after kidney transplant, as an “anti-rejection drug”/ immunosuppression. It belongs to a family of medications known as CNIs or calcineurin inhibitors. Cyclosporine is another example.
We don’t really know why tac specifically might cause hyperkalemia, but there are a few proposed mechanisms.
The pathway mechanisms lies in the distal convoluted tubular cells in the kidney. Calcineurin inhibition reduces mineralocorticoid receptors activity, which reduces the expression of Renal Outer Medullary Potassium (ROMK) channels, which reduces the excretion of potassium into the lumen. This pathway overlaps with why ACE and ARBs cause hyperkalemia, by reducing aldosterone activity, impacting the mineralocorticoid receptors, and reducing expression of ROMK.
This is a fancy way of saying that tac reduces potassium excretion in the urine!
What about other meds frequently seen post transplant?
Not associated with hyperkalemia:
- Sicromilus
- Everolimus
- Mycophenolic acid
- Azathioprine
- Belatcapet
- Prednisone
Associated with hyperkalemia:
- Cyclosporine
- Pentamidine
- Trimethoprim/sulfamethoxazole (TMP/SMX)
Have a question?
Send me an email! contact@kellypicard.com
appreciate the effort you put into getting us this information