Fludrocortisone Is an Effective Treatment for Hyperkalaemic Metabolic Acidosis in Kidney Transplant Recipients on Tacrolimus: A Case Series

Abstract

Background: Hyperkalaemia with metabolic acidosis is common but under-reported following kidney transplantation. Calcineurin inhibitors, such as tacrolimus, are widely used in the management of transplant patients and are associated with the development of hyperkalaemia. We report on 10 renal transplant patients, treated with fludrocortisone, following identification of hyperkalaemic metabolic acidosis. Results: All 10 patients were male aged (mean ± SD) 53.0 ± 13.2 years; 7 were Caucasian and 3 South Asian. Before and after fludrocortisone administration, respective (mean ± SD) serum potassium was 6.1 ± 0.4 mmol/L and 5.3 ± 0.3 mmol/L (p = 0.0002); serum bicarbonate 18.5 ± 1.6 mmol/L and 20.5 ± 2.3 mmol/L (p = 0.002); serum sodium 135 ± 4.6 mmol/L and 137 ± 2.2 mmol/L (p = 0.0728); serum creatinine 181 ± 61 μmol/L and 168 ± 64 μmol/L (p = 0.1318); eGFR 42 ± 18 mL/min and 46 ± 18 mL/min (p = 0.0303); blood tacrolimus 10.1 ± 2.9 ng/mL and 10.4 ± 1.4 ng/mL (p = 0.7975); and blood pressure 129 ± 15/79 ± 25 mm Hg and 126 ± 24/75 ± 7 mm Hg. Pre-fludrocortisone, there were 7 episodes of serum potassium ≥6.5 mEq/L, with 4 patients requiring admission for the treatment of hyperkalaemia. Following fludrocortisone, no patients had hyperkalaemia requiring inpatient management. Conclusions: Treatment of hyperkalaemic metabolic acidosis in transplant patients on tacrolimus with low-dose fludrocortisone resulted in rapid correction of hyperkalaemia and acidosis without significant effects on blood pressure or serum sodium. Fludrocortisone can be an effective short-term option for the treatment of hyperkalaemic metabolic acidosis in kidney transplant recipients on tacrolimus; however, patient selection remains important in order to reduce to risk of potential adverse effects.

Clinical and biological factors predisposing to hyperkalemic renal tubular acidosis in solid organ transplant recipients : a retrospective monocentric study

“…A 2022 case series report by Gama et al included 10 kidney transplant recipients in whom a short term low-dose udrocortisone therapy (50-100 µg daily) was introduced after failure of sodium bicarbonate therapy to treat hyperkalemic RTA. Fludrocortisone was found to be safe and effective, with no adverse effects on blood pressure, serum sodium, or volume status [29].…”

“…It is also common to initiate sodium bicarbonate supplementation in patients with hyperkalemic RTA. However, the bene t of this alkaline therapy appears to be limited in the treatment of patients with type 4 RTA [29,43,44].…”

“…Finally, udrocortisone has been used successfully in multiple case reports or case series in the treatment of refractory hyperkalemic RTA in transplant recipients [25,28,29]. Typically used dosages are 50 µg or 100 µg per day orally, and there is evidence that this molecule is also effective in situations of hyporeninism-hypoaldosteronism [45].…”

Hyperkalemia in Chronic Kidney Disease: Links, Risks and Management

“…[50][51][52][53] Fludrocortisone is a mineralocorticoid agonist that has shown some promise in small case series of hyperkalemic patients. [54][55][56] This is alluded to in the KDIGO guidelines but without any firm recommendations for use. Aldosterone has fibrotic effects on the cardiovascular system and kidneys and antagonism has led to an improvement in cardiovascular renal outcomes in the FIDELIO-DKD and FIGARO-DKD studies.…”

Type 4 renal tubular acidosis and uric acid nephrolithiasis: two faces of the same coin?

“…Congenital forms due to defects in adrenal steroidogenesis are much rarer conditions [40]. Furthermore, several medications which interfere with the RAAS have been associated with the development of type 4 RTA including angiotensin converting enzyme inhibitors, angiotensin receptor blockers, calcineurin inhibitors and heparin (Table 1) [41,42 ▪ ,43].…”