Key result
Spironolactone normalizes potassium and controls blood pressure in post-kidney transplant primary aldosteronism.
Why the study?
In patients with end-stage kidney disease and anuria, the renal effects of aldosterone may be attenuated, potentially masking classical biochemical manifestations of primary aldosteronism, which may be unmasked after kidney transplantation.
Case Report (n=1)
Prolonged anuria can mask the hypokalemic manifestation of primary aldosteronism, which may be unmasked by kidney transplantation, highlighting the need for targeted assessment in patients with recurrent hypokalemia post-transplant.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for primary aldosteronism in post-transplant hypokalemia; does not yet support routine screening or practice change.
Introduction Primary aldosteronism (PA) is a common cause of secondary hypertension and hypokalemia. In patients with end-stage kidney disease and anuria, however, the renal effects of aldosterone may be attenuated, potentially masking the classical biochemical manifestations of PA. Restoration of kidney function after transplantation may therefore unmask previously unrecognized PA. Case Presentation A 71-year-old man with a history of arterial hypertension and a remote episode of spontaneous hypokalemia progressed to end-stage kidney disease and remained anuric on maintenance hemodialysis for approximately 10 years. During dialysis, serum potassium levels remained within the normal range. Following deceased-donor kidney transplantation, graft function recovered with urine output exceeding 2 L/day, and severe hypokalemia (2.7 mmol/L) developed 14 days after transplantation despite normal serum sodium levels and in the absence of significant gastrointestinal or diuretic potassium losses. Endocrine evaluation revealed markedly elevated plasma aldosterone (260 ng/dL) and suppressed plasma renin activity (0.4 ng/mL/h), with an aldosterone-to-renin ratio of 650. Adrenal computed tomography demonstrated a 19-mm right adrenal nodule with an unenhanced attenuation value <10 Hounsfield units. Given the patient's age, comorbidities, and recent transplantation, adrenal venous sampling and surgery were not pursued, and treatment with spironolactone was initiated. At 3 months, serum potassium remained within the normal range with stable kidney allograft function and well-controlled blood pressure. Conclusion This case highlights the potential for prolonged anuria to mask the hypokalemic manifestation of PA and for kidney transplantation to unmask previously unrecognized aldosterone excess. Recurrent or unexplained hypokalemia after transplantation, particularly in patients with a history of hypokalemia or persistent hypertension before end-stage kidney disease, should prompt consideration of PA. Targeted assessment of aldosterone and renin may facilitate earlier diagnosis in selected kidney transplant recipients.
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Malatesta et al. (2026) conducted a case report in Primary aldosteronism (n=1). Spironolactone was evaluated on Serum potassium and blood pressure control. Treatment with spironolactone normalized serum potassium and controlled blood pressure at 3 months in a 71-year-old man whose primary aldosteronism was unmasked by kidney transplantation.
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