Endocrine Abstracts

Introduction: Chronic kidney disease (CKD) is associated with alterations in endogenous glucocorticoid regulation through various mechanisms: longer plasma cortisol half-life, reduced renal cortisol clearance, loss of 11b-HSD type 2 activity in the kidney contributing to an elevated cortisol/cortisone ratio, less effective hepatic metabolism of cortisol and, finally, hyperactivation of the hypothalamus-pituitary-adrenal axis due to acidosis, chronic stress, and inflammation.

Case report: We present the case of a 63-year-old woman, with cardiovascular, renal, and gastrointestinal comorbidities (arterial hypertension, heart failure, end-stage chronic kidney disease undergoing hemodialysis for 5 years, chronic hepatitis C) that was referred to the Endocrinology Department for uncontrolled blood pressure (220 mmHg) and an incidentally discovered right adrenal mass of 22/11 mm, with radiological features suggestive of adenoma. Clinical examination revealed a BMI of 33.9 kg/m², blood pressure of 160/80 mmHg, pale, dehydrated skin and anuria. Hormonal evaluation revealed normal 0800 h ACTH (21.5 pg/ml) and cortisol levels (19.8 μg/dl), normal free plasma metanephrine levels, elevated late-night salivary cortisol (LNSC):85.1 nmol/l (reference range, <11.3) and lack of suppression of serum cortisol on 1 mg, 2×2 mg and 8 mg dexamethasone suppression tests. DHEAS levels were in the low-normal range. Despite biological tests suggesting autonomous cortisol secretion, the patient did not exhibit glucose and lipid metabolism abnormalities (normal plasma glucose, HbA1c, lipid profile), therefore periodic follow-up was recommended. At one-year follow-up, biochemical testing showed a normal LNSC (8.5 nmol/l), normal 0800 h ACTH and cortisol and lack of adequate suppression after 8 mg overnight dexamethasone suppression (cortisol level of 5.79 μg/dl). Follow-up adrenal CT scan didn’t show any significant changes. In the absence of significant metabolic disturbances and considering the limitations of hypercortisolism assessment in CKD, we opted for periodical follow-up.

Discussions: One particular feature of investigating adrenal incidentalomas in dialysis patients is the difficulty to distinguish autonomous cortisol secretion from the impact of chronic kidney disease on cortisol metabolism. False-positive results may occur at screening investigations for hypercortisolism, such as late-night salivary cortisol or low-dose dexamethasone tests. In our case, a repeated value of LNSC within the normal range was not in favor of a definitive diagnosis of Cushing syndrome. More so, metabolic complications, such as dyslipidemia and glycemic abnormalities, were lacking. In such patients, clinical and biological follow-up and evaluation of comorbidities potentially attributable to cortisol excess (diabetes mellitus, dyslipidemia, osteoporosis) is recommended.