Disorders of sodium and water balance are frequently encountered in both the inpatient and outpatient setting, requiring a sound understanding of endocrine and renal physiology to properly diagnose and manage. Diabetes insipidus (DI) was recognised by the ancient Greeks but it was not until the early 20th century that its pathogenesis was elucidated. Central DI results from inadequate secretion of arginine vasopressin (AVP) from the posterior pituitary, while nephrogenic DI is a syndrome of renal AVP resistance. The common aetiologies of both forms of DI will be presented. Adipsic DI can be difficult to manage and carries an increased mortality. A standardised Australian protocol for the water deprivation test has been recently proposed; it is mainly used to differentiate partial central DI from primary polydipsia. The measurement of copeptin, the C-terminal fragment of proAVP, shows promise in the diagnosis of the polydipsia polyuria syndrome. It is low in central DI and raised in nephrogenic DI. This assay is being developed in some Australian pathology laboratories. The mainstay of treating central DI is oral or nasal desmopressin. Nephrogenic DI has been traditionally treated with diuretics (thiazide + amiloride) and/or non-steroidal anti-inflammatory drugs. Recent data show therapeutic potential for other drugs including metformin, simvastatin and sildenafil. New agents targeting the V2 receptor are being investigated. Hyponatraemia is common among hospital inpatients, and specialist Endocrine input has recently been shown to reduce time to Na correction and shorten length of hospitalisation. Urea in doses of 30-60g/day is a cheap and very effective therapy for the syndrome of inappropriate antidiuretic hormone (SIADH) that is poorly responsive to fluid restriction alone. Tolvaptan is now available in Australia but is not PBS-subsidised. It causes a prompt increase in serum Na but with a significant risk of overcorrection in real world practice.