These lecture notes accompany the MBChB Year 5 case-based tutorial on abnormal electrolytes (2025). They are an adjunct to the tutorial and may not make complete sense in isolation.
hyponatraemia is usually a problem of having too much body water
hyponatraemia can be a medical emergency
check POsm to confirm hypotonicity
check UOsm to ask if the ADH-kidney axis is responding appropriately
check UNa as a marker of volume status
Regulation of body water
Hyponatraemia is usually a problem of too much body water. We don’t routinely measure body water content and therefore excess water (low tonicity) is detected by finding a low plasma sodium level. Don’t let this trick you into thinking that hyponatraemia is caused by not enough body sodium. You will understand hyponatraemia best and make good clinical decisions if you think of it as too much body water.1 The reality is a bit more complicated. Strictly speaking hyponatraemia results from either not enough body solute - often approximated as total body sodium plus total body potassium - or too much body water. Google “Edelmen equation” to learn more about that if you are really keen!
Body water content is controlled in a negative-feedback loop in which anti-diuretic hormone ADH2 Anti-diuretic hormone; sometimes called vasopressin. is released from the posterior pituitary in reponse to rising plasma tonicity. ADH acts in the collecting ducts of the kidney, opposing the excretion of water in the urine. This system relies on the kidneys being able to excrete free water at a rate to match water intake:
Hyponatraemia can be a medical emergency
Severe acute hyponatraemia is a medical emergency because it can cause life-threatening cerebral oedema. This requires prompt treatment with hypertonic saline. Patients are also at risk of the osmotic demyelination syndrome if the hyponatraemia is corrected too quickly (almost always in the presence of additional risk factors: malnutrition, EtOH XS, hypokalaemia…).
Causes of hyponatraemia
Diagnosing the underlying cause is important in order to guide appropriate management. In addition to history and examination, the plasma osmolality (POsm), urine osmolality (UOsm) and urine sodium concentration (UNa) can help.
Remember why we check these investigations:3 Don’t fall into the trap of assuming that we check urinary sodium to see if renal sodium losses are causing hyponatraemia - remember this is a water problem, not a sodium problem!
We check:
POsm to confirm that this is a true hypotonic state (rather than translocational or pseudo- hypoNa)
UOsm to ask if the kidneys are responding appropriately to there being too much water: if there is intact ADH signalling and normal kidneys, UOsm should be low as the kidneys attempt to excrete the excess water
UNa as a surrogate - and sensitive4 UNa is more accurate that doctors at assessing volume status. Makes sense: the kidneys have evolved over millions of years to do this job. - marker of volume status: if the kidneys sense volume depletion (in real volume depletion or low-perfusion states such as heart failure) then the renin-angiotensin system will be activated, the renal tubules will hang on to salt and UNa will be low
Hyponatraemia may be caused by:
translocation of water into the circulation such as in severe hyperglycaemia (in which case plasma tonicity will be normal and there is no risk of cerebral oedema; POsm > 280 mOsm/L)
excessive water intake or low dietary solute intake (in which the urine will be very dilute: UOsm < 100 mOsm/L)
release of ADH in response to hypovolaemia (in which case the renin-angiotensin system will also be activated so that urinary sodium excretion is low: UNa < 30 mM)
release of ADH in response to what the body perceives as hypovolaemia in low cardiac-output or vasodilated states such as heart failure or portal hypertension (renin-angiotensin system will be activated so UNa < 30 mM)
inappropriate release of ADH in euvolaemia in response to drugs, pain, stress or as a paraneoplastic pheomenon = SiADH (UNa > 30 mM)
Additional reading
Core materials
The European joint society algorithm (figure 6 in guidelines) provides a really useful framework to work from. Worth looking at now and then consulting frequently in the years to come.
The European joint society full guidelines give a comprehensive overview of hyponatraemia but goes into much more detail than most doctors need to know (it is over 40 pages long).
One problem in this area is that there are multiple, conflicting guidelines which are neither quick nor easy to read.
This review article summarises key areas of agreement and disagreement in the major guidelines. Definitely well beyond the core curriculum.
