We describe a 78-year-old female patient with severe hyponatremia owing to inappropriate antidiuresis. Despite hyponatremia, the urinary sodium excretion persisted with urine osmolality exceeding plasma osmolality. Although a water load decreased plasma sodium concentration and osmolality, the patient excreted only 40% of the water load after 4 h without decreased urine sodium concentrations and osmolality. The plasma vasopressin levels relative to plasma osmolality were not inappropriately elevated. Intravenous administration of the selective nonpeptide vasopressin V2 antagonist OPC-31260 decreased sodium concentration and osmolality in urine to lower values than in plasma. Concomitantly, the urine volume excretion increased markedly. In addition, restriction of water or administration of demeclocycline improved plasma sodium and plasma vasopressin levels relative to plasma osmolality to be normal. The findings indicate that the inappropriate antidiuresis in this patient was related to hyperfunction of the arginine vasopressin V2 receptor in the kidney which is not due to inappropriately secreted vasopressin.