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Abstract: PO2582

Fludrocortisone Corrects Tacrolimus-Associated Hyperkalemia in Renal Transplant Patients

Session Information

Category: Transplantation

  • 1902 Transplantation: Clinical

Authors

  • Gama, Rouvick, Epsom and Saint Helier University Hospitals NHS Trust, London, United Kingdom
  • Quan, Virginia A., Epsom and Saint Helier University Hospitals NHS Trust, London, United Kingdom
  • Phanish, Mysore K., Epsom and Saint Helier University Hospitals NHS Trust, London, United Kingdom
Background

Hyperkalemic metabolic acidosis is commonly observed following kidney transplantation. This is often due to calcineurin inhibitors which are known to cause type 4 renal tubular acidosis either due to hyporeninemic hypoaldosteronism or due to direct effect on aldosterone responsive potassium secretion in the distal nephron.

Methods

We report 5 post-renal transplant patients (5 males) on tacrolimus with hyperkalemia treated with daily doses of either 50 mcg (n=3) or 100 mcg (n=2) of fludrocortisone. We retrospectively collected data at 3 time points before and after fludrocortisone on serum concentrations of sodium, potassium, bicarbonate, creatinine and tacrolimus as well as eGFR and blood pressure (BP). We recorded emergency admissions and length of stay (LoS) for treatment related to hyperkalemia. Data are presented as mean +/-SD and analysed with a paired students t-test.

Results

Pre and post-fludrocortisone serum concentrations for potassium was 6.3 ± 0.3 mmol/L and 5.1 ± 0.3 mmol/L (p=0.002); venous bicarbonate 18.4 ± 1.8 mmol/L and 20.4 ± 2.0 mmol/L (p=0.108); sodium 135 ± 1.6 mmol/L and 135 ± 2.2 mmol/L (p=0.875); creatinine 184 ± 12.2 mmol/L and 155 ± 10.6 mmol/L (p=0.058); eGFR 39 ± 3.4 ml/min and 47 ± 4.2 ml/min (p=0.035); blood tacrolimus levels 9.8 ± 2.1 ng/mL and 11.2 ± 1.0 ng/mL; BP was 133/69 ± 12/9 mmHg and 129/70 ± 8/6 mmHg before and after fludrocortisone respectively. We were able to either reduce or stop sodium bicarbonate after starting fludrocortisone due to increase in serum bicarbonate levels.

Prior to fludrocortisone there were 6 episodes of serum potassium greater than 6.5 mEq/L, of which 3 patients required admission for hyperkalaemia management, with LoS 1-3 days. The majority occurred with tacrolimus levels in target range. Reduction in potassium levels to ‘safe levels’ were noted within 24-48 hours of starting fludrocortisone.

Conclusion

Treatment of hyperkalemic metabolic acidosis with fludrocortisone resulted in rapid normalization of serum potassium. There were no adverse effects on BP, serum sodium levels or clinical evidence of fluid retention. Instigation of fludrocortisone prevented emergency admissions for treatment of hyperkalemia and allowed the clinicians to run adequate tacrolimus levels. Fludrocortisone can be a cheap, safe and effective option for the treatment of hyperkalemia in renal transplant patients on tacrolimus.