Other pituitary disorders and kidney disease

Abstract

Prolactin (PRL) levels are elevated in chronic kidney disease (CKD) due to reduced clearance and increased secretion. Hyperprolactinemia manifests as galactorrhea and hypogonadism. Treatment of hyperprolactinemia should focus on improving bothersome galactorrhea or hypogonadism by using dopamine agonists and replacement of sex hormone(s). Changes in the hypothalamic-pituitary-adrenal (HPA) axis in CKD are characterized by increases in adrenocorticotropic hormone (ACTH) and sometimes cortisol levels, largely preserved circadian rhythms of ACTH and cortisol, and a normal response of cortisol to ACTH, metyrapone, and insulin-induced hypoglycemia. However, the HPA axis is less inhibited by 1 mg of dexamethasone but retains normal suppression by higher-dose dexamethasone. Diagnosis of adrenal insufficiency in CKD patients, as in normal subjects, is usually made by finding a subnormal cortisol response to ACTH. The mainstay of treatment of adrenal insufficiency is to replace glucocorticoid hormone. Cushing’s disease in CKD is difficult to diagnose and relies on the dexamethasone suppression test and the midnight salivary cortisol test since 24-h urine-free cortisol test is not useful. Treatment of Cushing’s disease involves surgery, complemented by radiation and/or medical therapy if necessary. In CKD, arginine vasopressin (AVP) levels are elevated due to decreased clearance, and there is also impairment of AVP signaling in renal tubules. Diabetes insipidus can be masked in advanced kidney disease until kidney transplantation. Diagnosis of syndrome of inappropriate antidiuretic hormone is similar in mild or moderate kidney disease as in normal subjects but is challenging in those with advanced kidney disease owing to the impairment in urine dilution.