Total body water is finely regulated and controls of intake and output are maximally activated by small osmotic changes. Sensors in the hypothalamus invoke the fluid repletion or depletion reactions through changes in thirst, urine concentration and solute intake. Antidiuretic hormone controls urinary concentration and is released mainly in response to osmotic stimuli. However, the threshold and sensitivity of this response are affected by non osmotic stimuli. Urine concentration varies in response to antidiuretic hormone only if the distal tubule, collecting duct and hypertonic medullary interstitum are intact. The capacity to conserve or excrete water depends on the osmolar load and an efficient urinary concentrating or diluting mechanism. Disorders of thirst are uncommon and often associated with abnormal antidiuretic hormone secretion. Disorders of urine concentration and dilution are common in illness and reflect abnormalities of antidiuretic hormone secretion or the renal mechanisms generating the osmotic gradient. When urine concentrating capacity is impaired ( true or nephrogenic diabetes insipidus) water depletion occurs only when thirst fails or access to water is denied. When urine diluting ability is impaired, water excess occurs when the osmolar load and minimum urinary osmolality generated are inadequate for the fluid intake. Hyper-osmolality and hypo-osmolality are usually caused by abnormal water metabolism although they may be associated with abnormalities of solute metabolism. The various clinical syndromes are determined by the primary disease, and the associated fluid volume and osmolar abnormalities.