Endocrine Abstracts

Introduction: Primary aldosteronism (PA) accounts for 20% of patients with resistant hypertension and is one of its leading causes. Options of treatment include adrenalectomy and mineralocorticoid receptor antagonists (MRAs). Latest studies suggest that both may paradoxically lead to a decline in estimated glomerular filtration rate (eGFR), explained by the masked glomerular hyperfiltration associated to PA before treatment.

Case report: A 56 years old male patient, presented in 2010 in Italy for resistant arterial hypertension associated with hypokalemia. Further biological tests revealed elevated aldosterone level associated with low plasma renin activity and the CT scan confirmed the diagnosis of PA: right adrenal hyperplasia and two solid lesions on the left one, both with a diameter of 10 mm. The adrenal vein sampling showed no lateralization, therefore chronic treatment with MRA (canrenone, 200 mg/d) was initiated with favorable response, but pacient failed to attend revaluation. After 8 years, while presenting in our department for the investigations of a toxic nodular goiter, the laboratory testing showed severe hyperkalemia (7.4 mmol/l), hematuria, proteinuria and reduced eGFR (9.2 ml/min per 1.73 m²). He was directed to a nephrology clinic where an abdominal ultrasound showed slightly reduced renal dimensions and the renal biopsy revealed 80% fibrosis and extensive lesions of arteriosclerosis, confirming the hypertensive etiology. At that time the patient was using multiple drugs, including canrenone 200 mg/d and furosemide 20 mg/d, hence the first step was to interrupt the latest and to start a low potassium diet. Further evaluations showed normal potasium and stationary eGFR and treatment with a low dose of Spironolactone (25 mg) was initiated, in order to reduce the risk of myocardial and renal fibrosis. A new CT scan was performed, this time revealing normal right adrenal gland and two adenomas (4.5 mm, respectivelly 10 mm in diameter) on the left one.

Discussion: This case supports the hypothesis that high levels of aldosterone lead to glomerular hyperfiltration. Multiple studies suggest pretreatment parameters like high plasma aldosterone, low plasma renin, low plasma potassium, and high eGFR are significant predictors of eGFR decline after start of treatment, also supported by our case. An explanation for the normokalemia at the present moment could be the balanced hypokalemia of primary aldosteronism with hyperkalemia of chronic renal failure. Despite normal levels of potasium and the diagnosis of chronic kidney disease, we recommend an interdisciplinary team evaluating the necesity of treatment with MRAs.