ESPE Abstracts (2021) 94 P2-29

ESPE2021 ePoster Category 2 Adrenals and HPA Axis (57 abstracts)

Fludrocortisone is the salvage treatment in cases with calcineurin inhibitor related hyperkalemia

Yagmur Unsal 1 , Demet Baltu 2 , Bora Gulhan 2 , Fatma Visal Okur 3 , Ali Duzova 2 , Alev Ozon 1 , Rezan Topaloğlu 2 & Nazlı Gonc 1

1Hacettepe University Pediatric Endocrinology, Ankara, Turkey; 2Hacettepe University Pediatric Nephrology, Ankara, Turkey; 3Hacettepe University Pediatric Hematology, Ankara, Turkey

Calcineurin inhibitors (CNIs) are widely used in pediatric transplantation for prevention of graft rejection, prophylaxis and treatment of graft versus host disease. Though hyperkalemia is a common adverse effect (10-45%), alterations in renin-angiotensin-aldosterone system in CNI-induced hyperkalemia are not well elucidated. Consequently, CNIs vital to transplantation are usually switched. Here, we describe two cases with CNI-induced hyperkalemia due to hyporeninemic hypoaldosteronism (HH), successfully treated with fludrocortisone. 15-month-old boy was diagnosed with acute myeloid leukemia and BFM-2013 protocol was started. When he was 22 months old, allogenic bone marrow transplantation was performed, cyclosporine (CsA) (3 mg/kg/day) was initiated on day -1, as preparative regimen. On day +22, hyperkalemia (5.9 mEq/L) and hyponatremia (133 mEq/L) were observed. He was normotensive, was not receiving intravenous fluid or potassium and hemolysis was ruled out. Serum chloride, blood urea nitrogen and creatinine were 103 mEq/L, 23.2 mg/dl, 0.5 mg/dl, respectively. Urinary sodium and potassium were 50.6 mEq/L and 6.3 mEq/L. Concomittant renin was 1.3 pg/ml (1.3-13.8), aldosterone was 71 pg/ml (35-300). Glucocorticoid deficiency (cortisol: 28 mcg/dl) or metabolic acidosis were not detected. Hyperkalemia was attributed to CsA related HH. Fludrocortisone 0.05 mg/day was started, and serum potassium decreased from 5.9 mEq/L to 3.8 mEq/L. CsA was continued for 6 months, following cessation, fludrocortisone was tempered and ceased, electrolyte imbalance was not observed. 3-year-old girl who underwent cadaver donor renal transplantation because of agenesis of the left kidney and cystic right kidney due to HNF1 beta mutation was started with CsA. Due to hypertrichosis, CsA was switched to tacrolimus. When she was 5 years old, hyperkalemia (7.37 mmol/l) and hyponatremia (128 mEq/L) were detected. Serum creatinine increased from 0.41 to 0.67 mg/dl, urinary sodium was 52.8 mEq/L and potassium was 13.89 mEq/L, serum renin and aldosterone were 1.18 pg/ml (1.3-13.8) and 47 pg/ml (35-300), respectively. Tacrolimus related HH was diagnosed and 0.05 mg fludrocortisone was initiated, serum potassium, sodium, and creatine were normalized within three days. The patient has been receiving fludrocortisone without dose adjustment for three years without electrolyte imbalance. HH is established as the underlying mechanism of CNI-induced hyperkalemia. If hyperkalemia is detected in cases using CNIs, renin and aldosterone should be measured. Fludrocortisone is a safe and effective treatment for CNI-induced hyperkalemia. It also provides maintaining CNIs fundamental to pediatric transplantation.

Volume 94

59th Annual ESPE (ESPE 2021 Online)

22 Sep 2021 - 26 Sep 2021

European Society for Paediatric Endocrinology 

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