Although more common with tacrolimus, it is known that calcineurin inhibitors may induce the development of electrolyte disorders such as hyponatremia and hyperkalemia by causing a hyporeninemic hypoaldosteronism-like syndrome. We present a 32-year-old female renal transplant patient who admitted to clinic with hyponatremia and hyperkalemia. Normal anion gap metabolic acidosis and renal tubular dysfunction were detected and after other reasons were excluded, it was considered as electrolyte disorder due to tacrolimus. No response was detected after tacrolimus conversion to everolimus and considering tubular dysfunction due to aldosterone resistance, we initiated fludrocortisone therapy and electrolyte disorders rapidly improved. Fludrocortisone therapy should be considered when hyponatremia and/or hyperkalemia due to tacrolimus are detected in renal transplant patients.