Changes in magnesium and potassium homeostasis after conversion from a calcineurin inhibitor regimen to an mTOR inhibitor-based regimen

Background: Transplant recipients treated with calcineurin inhibitors (CNIs) frequently show hyperkalemia, metabolic acidosis, and hypomagnesemia which could be deleterious for some patients. Conversion to inhibitors of mammalian target of rapamycin (mTOR) could improve these electrolytic disturbances.

Objective: To evaluate the potassium and magnesium changes due to converting patients from CNIs to mTOR inhibitors.

Methods: Retrospective review of 138 renal transplant patients who were converted from CNIs to mTOR inhibitors over a 6-month observation period. The following parameters were determined: potassium, sodium, chloride, magnesium, urea, glucose, and creatinine in blood and urine. We also analyzed plasma bicarbonate and calculated plasma and urine anion gap and plasma osmolarity.

Results: One month after conversion, a decrease was observed in serum creatinine (1.75±0.68 vs 1.61±0.61 mg/dL; P=.01), plasma potassium (4.60±0.52 vs 4.39±0.53 mEq/L; P<.001), calculated plasma osmolarity (308.7±8.5 vs 307.4±8.4 mOsm/L; P<.036), fractional excretion of sodium (1.55±0.69 vs 1.29±0.65%; P<.003), and fractional excretion of magnesium (7.15±4.08 vs 15.84±3.64%; P<.001), with an increase in serum magnesium (1.77±0.24 vs 1.95±0.29 mg/dL; P<.001). At 3 and 6 months, these differences remained unchanged. The transtubular potassium gradient did not change.

Conclusions: We observed a decrease in serum magnesium due to renal magnesium wasting before switching from CNIs to mTOR inhibitors. After conversion, an increase in serum magnesium was observed together with a drop in the fractional excretion of this cation. A decrease in plasma potassium levels, plasma osmolarity, and fractional excretion of sodium consistent with minor aldosterone resistance was also detected after changing the immunosuppressive treatment.