Clinical analysis of hyperkalemic renal tubular acidosis caused by calcineurin inhibitors in solid organ transplant recipients

Lin, Wanbing; Mou, Lijun; Tu, Hai‐Yan; Zhu, Lingjun; Wang, J.; Chen, J.; Hu, Yangmin

doi:10.1111/jcpt.12485

Cited by 13 publications

(8 citation statements)

References 16 publications

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“…1b). All patients were on tacrolimus, which is the most likely causative agent in keeping with previous studies, which have reported type-4 RTA in patients on tacrolimus following solid organ transplants [18][19][20]. An observational study involving 106 transplant patients on CNIs reported the prevalence of type-4 RTA to be 30.9%.…”

Section: Discussionsupporting

confidence: 66%

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

Gama¹,

Makanjuola²,

Wahba³

et al. 2021

Nephron

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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.

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Section: Discussionsupporting

confidence: 66%

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

Gama¹,

Makanjuola²,

Wahba³

et al. 2021

Nephron

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“…There remains an ongoing debate regarding the development of tubulopathies post‐renal transplantation with perhaps under recognition in clinical practice. Acute nephrotoxic injuries certainly contribute in many cases; however, CNI‐based immunosuppressive regimens are certainly recognized to cause tubular dysfunction . Renal transplant patients treated with CNIs such as ciclosporin A and tacrolimus (FK 506) may develop signs of partial resistance to aldosterone action with subsequent hyperkalaemia and metabolic acidosis, thus partially explaining the mechanism of action of fludrocortisone in this setting.…”

Section: Discussionmentioning

confidence: 99%

“…However, the incidence of this type 4 renal tubular acidosis remains unknown. Whilst tubular dysfunction can occur secondary to renal impairment and interstitial damage from acute episodes and nephrotoxic drugs, immunosuppressive regimens namely CNI (ciclosporin, tacrolimus) have also been directly implicated . These drugs are thought to lead to a down regulation of the mineralocorticoid receptors and a resultant pseudohypoaldosteronism picture with normal aldosterone levels.…”

Section: Introductionmentioning

confidence: 99%

Fludrocortisone—a treatment for tubulopathy post‐paediatric renal transplantation: A national paediatric nephrology unit experience

Ali

Shaheen

Young

et al. 2018

Pediatric Transplantation

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Calcineurin inhibitors post-renal transplantation are recognized to cause tubulopathies in the form of hyponatremia, hyperkalemia, and acidosis. Sodium supplementation may be required, increasing medication burden and potentially resulting in poor compliance. Fludrocortisone has been beneficial in addressing tubulopathies in adult studies, with limited paediatric data available. A retrospective review of data from an electronic renal database from December 2014 to January 2016 was carried out. Forty-seven post-transplant patients were reviewed with 23 (49%) patients on sodium chloride or bicarbonate. Nine patients, aged 8.3 years (range 4.9-16.4), commenced fludrocortisone 22 months (range 1-80) after transplant and were followed up for 9 months (range 2-20). All patients stopped sodium bicarbonate; all had a reduction or no increase in total daily doses of sodium chloride. Potassium levels were significantly lower on fludrocortisone, 5.2 vs 4.5 mmol/L, P = .04. No difference was noted in renal function (eGFR 77.8 vs 81.7 mL/min/1.73 m , P = .45) and no significant increase in systolic blood pressure (z-scores 0.99 vs 0.85, P = .92). No side effects secondary to treatment with fludrocortisone were reported. A significant proportion of renal transplant patients were on sodium supplementation and fludrocortisone reduced sodium supplementation without significant effects on renal function or blood pressure. Fludrocortisone appears to be safe and effective for tubulopathies in children post-transplantation.

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“…This phenomenon has only been described in rare cases following liver transplantation [5–7]. Patients with type IV RTA tend to be asymptomatic with normal creatinine and urine output.…”

Section: Discussionmentioning

confidence: 99%

Tacrolimus-Induced Type IV Renal Tubular Acidosis following Liver Transplantation

Schmoyer

Mishra

Fulco

2017

Case Reports in Hepatology

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Calcineurin inhibitors remain an integral component of immunosuppressive therapy regimens following solid organ transplantation. Although nephrotoxicity associated with these agents is well documented, type IV renal tubular acidosis is a rare and potentially underreported complication following liver transplantation. Hepatologists must be able to recognize this adverse effect as it can lead to fatal hyperkalemia. We describe a case of tacrolimus-induced hyperkalemic type IV renal tubular acidosis in a patient following an orthotopic liver transplant for alcoholic cirrhosis.

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Clinical analysis of hyperkalemic renal tubular acidosis caused by calcineurin inhibitors in solid organ transplant recipients

Abstract: We should alert for CNI-induced hyperkalemic RTA in transplant recipients. By CNI dosage reduction or adding low dose fludrocortisone, or temporarily switching to SRL, the prognosis of CNI-induced hyperkalemic RTA is favourable.

Cited by 13 publications

References 16 publications

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

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

Fludrocortisone—a treatment for tubulopathy post‐paediatric renal transplantation: A national paediatric nephrology unit experience

Tacrolimus-Induced Type IV Renal Tubular Acidosis following Liver Transplantation

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