HYPORENINAEMIC HYPOALDOSTERONISM (HH) AS THE CAUSE OF UNEXPLAINED HYPERKALAEMIA
DOI:
https://doi.org/10.15605/jafes.040.S1.027Keywords:
hypoaldosteronism, hyperkalaemia, diabetes, chronic kidney diseaseAbstract
INTRODUCTION
Hyporeninaemic hypoaldosteronism (HH) is a frequently overlooked cause of hyperkalaemia. In HH, juxtaglomerular apparatus dysfunction secondary to diabetes, chronic kidney disease and medications like NSAIDs, ACEI, and heparin leads to reduced renin secretion, thus decreasing aldosterone synthesis, resulting to impaired potassium excretion and H⁺ secretion. Hyperkalaemia and metabolic acidosis ensue respectively with no adrenal insufficiency.
CASE
A 57-year-old female presented with persistent and asymptomatic hyperkalaemia for a year at primary care. Hemolysis was ruled out. Electrocardiogram findings remained normal throughout. She had type 2 diabetes mellitus for 15 years, hypertension and stage 2 chronic kidney disease (CKD) (eGFR ~62 mL/min/1.73 m²) for 2 years. Diabetes was moderately controlled with metformin. Hypertension was treated with amlodipine. Additionally, she had been using NSAIDs intermittently for back pain over the last three years. Due to the presence of hyperkalaemia despite the fairly normal renal function, she was referred to an endocrinologist. Further evaluation included a morning serum cortisol level at 9 am, which was normal, ruling out adrenal insufficiency. However, serum aldosterone was low with inappropriately low renin levels despite elevated potassium. Mild metabolic acidosis was present. These findings strongly suggested a diagnosis of HH. The patient was managed through dietary potassium restriction, discontinuation of NSAIDs, initiation of fludrocortisone for potassium excretion, and sodium bicarbonate to correct the metabolic acidosis with a close watch on renal function and potassium levels. Within two weeks, her potassium levels normalized and remained stable thereafter. Hyperkalaemia was ultimately attributed to HH, likely caused by a combination of chronic diabetes with CKD and the use of NSAIDs, all leading to juxtaglomerular apparatus dysfunction.
CONCLUSION
This case highlights the importance of considering HH in persons with diabetes or CKD with unexplained hyperkalaemia despite a normal or mildly impaired renal function and initiating the appropriate management to prevent potentially life-threatening arrhythmias.
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Copyright (c) 2025 Ashok Veerappan, Nishkkriyaa Gopal, Valliammai Valliyappan

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