Endocrine Abstracts

Introduction: Central and Peripheral Diabetes Insipidus are both rare conditions. Combined they may result in serious hypernatremia and water deficit that may pose a therapeutic challenge.

Case report: MHBCR, a caucasian female aged 52, was admitted to the Endocrine Department because of serious hypernatremia. A previous diagnosis of pituitary failure and central diabetes insipidus was established 4 years before, after pituitary surgery for a non-secreting pituitary adenoma and was treated with hydrocortisone 20+5+5 mg/day, L-thyroxine 125 μg/day and desmopressin 60 μg/day po and 80 μg/day intranasal. Because of an acute psychotic episode she was medicated with lithium 400 mg/day, 7 days before. On admission hypernatremia was found (153 mEq/l), with normal serum potassium and renal function. Urine output was 12 400 ml/day. Litium was interrupted, fluid i.v. administration was increased up to 6000 ml/day (normal and hypotonic saline), desmopressin 4 μg, i.v. 12/12 h, hydroclorothiazide 50 mg/day and indometacin 400 mg/day were initiated. In the next few days, urine output decreased to 6–7 l, water balance was almost null, with normal urea, but serum sodium increased to 180 mEq/day. Desmopressin was increased up to 4 μg, i.v. 4/4 h but was ineffective. Dialysis was begun at the seventh intra-hospital day with correction of serum sodium to 160 mEq/l in a single session. Furosemide 40 mg/day, i.v. further normalized serum sodium to 132 mEq/l in the next few days.

Discussion: Combined central and peripheral diabetes insipidus may result in serious life-threatening hypernatremia because of massive water loss. In this case both conditions were conventionally treated but despite no evidence of hemoconcentration, sodium further increased in a dramatic way, pointing to a specific sodium excretion defect. The most likely explanation is increased renin–angiotensin–aldosterone activity because of volume depletion with increased distal tubule reabsorption of sodium. This possibility is supported by the transient nature of the defect and the very good response to furosemide.