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Endocrine Abstracts (2025) 110 P155 | DOI: 10.1530/endoabs.110.P155

ECEESPE2025 Poster Presentations Adrenal and Cardiovascular Endocrinology (169 abstracts)

Post adrenalectomy hyperkalemia in primary aldosteronism. A case series of a not well-defined complication

Carlien de Herdt 1 , Pieter-Jan Van Gaal 2 , Christophe De Block 1 & Eric Gheuens 2


1Antwerp University Hospital, Endocrinology, diabetology and metabolic diseases, Edegem, Belgium; 2ZAS Cadix, Nephrology, Antwerp, Belgium


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Introduction: Hyperkalemia post adrenalectomy can develop in primary aldosteronism (PA) due to chronic suppression of renin–angiotensin–aldosterone system (RAAS). There is too much uncertainties concerning this complication in terms of prevalence, risk factors, aetiology and treatment. We present the postoperative course of PA cases who underwent adrenalectomy.

Methodology: Inclusion of cases with unilateral PA confirmed by adrenal venous sampling (at the Antwerp University Hospital) who underwent unilateral adrenalectomy. Blood results were retrospectively evaluated 1–4 weeks and 2–12 months postoperatively.

Results: 13 cases (M=9) with a mean age of 56±11 years were included. 3 cases developed hyperkalemia < 4 weeks postoperatively and persisted in 2 cases. Both were men, had a history of arterial hypertension > 10 years and a normal kidney function. One case had a preoperatively hypokalemia. The first case developed a grade 3 hyponatremia and grade 1 hyperkalemia with a 45% increase of the serum creatinine level. Plasma aldosterone and renin levels were low. Kidney function and potassium level normalized under treatment with Kayexalate, but hyponatremia and suppression of RAAS persisted. The second case developed a grade 2 hyperkalemia and grade 3 hyponatremia with a 75% increase of the serum creatinine. Under treatment with Fludrocortisone, potassium and sodium levels improved. Plasma aldosterone was low-normal with an inappropriate normal renin level. Early postoperative suppression of RAAS was present in 5/13 cases and led to hyperkalemia in 2 cases. In the 3 cases without electrolyte disturbances, RAAS recovered.

Conclusion: Post adrenalectomy hyperkalemia in PA is stated to be a well–documented entity with a variable prevalence (4.5–7%). In our cohort of 13 cases, 1 case had a transient and 2 cases persistent hyperkalemia. Both cases with persistent electrolyte disturbances had a suppression of RAAS. Risk factors described in the literature and met by these 2 cases were older age (>53 years) and longer duration of hypertension. Early postoperative, 5/13 cases had a suppression of RAAS, leading to hyperkalemia in only 2 cases. Reviewing the literature, there is no difference in early postoperative plasma aldosterone or renin levels in cases with and without hyperkalemia. However, case series are small (largest including 9 cases with persistent postoperative hyperkalemia) and timing of blood sample varies. It is unknown why in most cases, postoperative suppression of RAAS is not associated with hyperkalemia. We state post adrenalectomy hyperkalemia is a not well-documented entity. Larger case series are needed to compare cases with and without post adrenalectomy hyperkalemia.

Volume 110

Joint Congress of the European Society for Paediatric Endocrinology (ESPE) and the European Society of Endocrinology (ESE) 2025: Connecting Endocrinology Across the Life Course

European Society of Endocrinology 
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