A 58-year-old male patient with a history of hypertension presented with abdominal pain and nausea. Five months previously, he had presented with dyspnoea, abdominal fullness and pretibial oedema and was hospitalised in the coronary intensive care unit with the diagnosis of decompensated heart failure. At that time, renal function and serum sodium and potassium levels were completely normal. Low-dose aspirin, propranolol, nitrate, frusemide (furosemide), amiodarone and spironolactone were prescribed. At the last admission to our hospital, his body temperature was 36°C, blood pressure was 140 ⁄ 100 mm Hg, heart rate was 100 ⁄ min, regular. He was orientated and co-operative. Skin was normal, external jugular veins were not engorged. On auscultation of chest, there were bilateral crepitations. The heart was tachycardic and arrhythmic with no murmurs heard. No organomegaly or tenderness were found. Peripheral pulses were palpable in all extremities; there was no pretibial oedema. Laboratory findings were as follows: white blood cell, 11.900; haematocrit, 42.1; MCV, 83.9; platelets, 278.000; serum Na, 107 mEq ⁄ l; serum K, 4.1 mEq ⁄ l; blood urea nitrogen, 14 mg ⁄ dl; Creatinine, 1.0 mg ⁄ dl; total protein, 7.1 g ⁄ dl; albumin, 4.5 g ⁄ dl; TSH 0.76; free T3, 2.8; free T4, 2.6; CRP 3.1; uric acid, 2.7 mg ⁄ dl; AST, 36 IU ⁄ l; ALT, 32 IU ⁄ l; LDH, 499; urinary Na, 31 mEq ⁄ l; urinary osmolarity, 677. Blood lipids were within normal limits. On ultrasound, both kidneys were within the normal range with a simple renal cyst on the left kidney. There was mucosal thickening of the bladder wall with increased trabeculation. On transthoracic echocardiography, ejection fraction (EF) was 63% with dilatation of left atrial, right atrial and ventricular, 1 ⁄ 2 mitral regurgitation, 1 ⁄ 2 tricuspid regurgitation and mild pulmonary hypertension.Our primary diagnosis of syndrome of inappropriate antidiuretic hormone secretion (SIADH) was based on hyponatremia, high urinary osmolarity, high-normal urinary Na, hypouric acidemia and absence of hypervolemia. But the aetiology was not apparent. Limiting the water and salt intake did not correct the serum Na level. Although malignancy was a well-known cause of SIADH, there was no abnormality on routine X-ray and ultrasound to suggest further examinations, such as CT or MR scanning. With the suspicion of druginduced SIADH, we discontinued amiodarone and observed the patient. Because he was asymptomatic, we discharged him with serum Na of 117 mEq ⁄ l. One and two weeks later in the outpatient clinic, serum Na levels were 123 and 130 mEq ⁄ l, respectively.A review of the literature revealed four case reports of SIADH-induced hyponatremia associated with amiodarone treatment between 1999 and 2004. In two of them, hyponatremia developed during the loading dose of amiodarone treatment and responded well to dose reduction without discontinuation of drug (1, 2). In one of these cases, the serum Na level was improved within 3 weeks of dose reduction (1). In a 67-year-old male patient with multiple ...