[Hyponatremias: From pathophysiology to treatments. Review for clinicians]

Hyponatremia could be defined as a public health topic: too many patients are concerned in both hospitalized and general populations; hyponatremia induces lots of clinical outcomes and a great economic burden. Its pathophysiology involves thirst regulation (hypotonic water intakes) and losses regulation (through the kidney under vasopressin control). Diagnostic approach should insure that hyponatremia reflects hypo-osmolality and hypotonicity: first, a false hyponatremia should be ruled out, then a non-hypotonic one. Next step is clinic: extracellular status should be evaluated. When increased, any edematous status should be evoked: heart failure, liver cirrhosis or nephrotic syndrome. When decreased, any cause of extracellular dehydration should be evoked: natriuresis could help distinguishing between renal (adrenal insufficiency, diuretics use or salt-losing nephropathy) or extrarenal (digestive mostly) etiologies. When clinically normal, a secretion of inappropriate antidiuretic hormone (SIADH) should be evoked, once hypothyroidism or hypoadrenocorticism have been ruled out. Therapy depends on the severity of the clinical impact. From extracellular rehydration, through fluid restriction, the paraneoplastic and heart failure-induced SIADH benefit from a new class of drug, available among the therapeutic strategies: aquaretics act through antidiuretic hormone receptor antagonism (vaptans). Their long-term benefits still have to be proven but it is a significant step forward in the treatment of hyponatremias.