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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Nephrocalcinosis is an important imaging finding but is often overlooked, and its underlying causes are diverse. Disorders associated with nephrocalcinosis include transporter abnormalities such as Liddle syndrome, autoimmune-related tulointerstitial nephritis, and primary aldosteronism, all of which can induce hypokalemia. Hypercalcemia is also known to cause nephrocalcinosis and renal impairment.Conversely, conditions combining obesity and hypocalcemia are typically linked to hormonal disorders such as Cushing’s syndrome; however, reports of nephrocalcinosis in endocrine disorders remain scarce. We report a case of an obese woman presenting with persistent hypokalemia, hypertension, hypocalcemia, recurrent fatigue, and nephrocalcinosis at the corticomedullary junction, initially suspected as Cushing’s syndrome but later found to have low ACTH and cortisol levels.
A 45-year-old woman (BMI 32.6 kg/m²) presented with recurrent muscle weakness and persistent hypokalemia despite potassium supplementation. Blood pressure was 137/86 mmHg without spironolactone. Laboratory tests revealed low plasma renin and normal aldosterone levels. Abdominal CT showed no adrenal adenoma but demonstrated multiple faint calcifications at the renal corticomedullary junction. Rapid ACTH stimulation test showed normal cortisol responsiveness. She had no history of congenital adrenal hyperplasia, malignancy, vomiting, or autoimmune disease. Despite potassium replacement, hypokalemia and metabolic alkalosis persisted, accompanied by hypocalcemia. Spironolactone therapy was initiated, resulting in marked improvement in serum potassium, muscle weakness, and appetite within three weeks. Blood pressure normalized without calcium channel blockers. Repeated endocrine evaluations revealed low ACTH and cortisol but no definitive etiology; urinary cortisol/cortisone ratio was not assessed.
In obesity, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activity is upregulated in visceral adipocytes, enhancing intracellular glucocorticoid reactivation. Local cortisol action is tightly regulated by the balance between 11β-HSD1 and the inactivating enzyme 11β-HSD2. In this patient, severe obesity likely increased 11β-HSD1 activity, while adipocytes lack 11β-HSD2, potentially leading to local glucocorticoid excess despite low systemic cortisol. This mechanism may explain the paradoxical combination of obesity, low ACTH/cortisol, and mineralocorticoid receptor activation, resulting in hypokalemia and hypertension.This case highlights that in patients with nephrocalcinosis without autoimmune disease, endocrine abnormalities—particularly obesity-related tubular dysfunction and hypokalemia—should be considered.
Nephrocalcinosis in the setting of obesity and persistent hypokalemia warrants evaluation for local glucocorticoid dysregulation, even in the absence of systemic hypercortisolism.
