Hyponatraemia is the most common electrolyte disorder, affecting more than 15% of patients in hospital – and is also frequently seen in the outpatient setting, especially among older adults. Chronic hyponatremia is associated with impaired cognition, increased falls and fractures, and increased mortality.
The syndrome of inappropriate anti-diuresis (SIAD) is the most frequent cause of hypotonic hyponatraemia, mediated by non-osmotic release of arginine vasopressin (AVP, previously known as anti-diuretic hormone (ADH)) which acts on the renal V2 receptors to promote water retention. Several differentials should be excluded before a diagnosis of SIAD is made, including adrenal insufficiency and diuretic effect. There are a variety of underlying causes of SIAD, including malignancy, pulmonary pathology and central nervous system pathology, or it may be deemed idiopathic. n clinical practice, the aetiology of hyponatraemia is frequently multifactorial.
In the absence of severe symptoms requiring urgent intervention, fluid restriction is widely endorsed as first line treatment for SIAD in current guidelines, but there is controversy regarding second line therapy in instances where fluid restriction is unsuccessful, which occurs in around half of cases.
I review the epidemiology, pathophysiology and differential diagnosis of chronic hyponatraemia, and summarise recent evidence for therapies for SIAD beyond fluid restriction, with a focus on tolvaptan, urea and sodium-glucose co-transporter 2 inhibitors (SGLT2i).