The main stimulus for ADH secretion is a low "effective" vascular volume or low ECF volume. This will also stimulate the "thirst" centre, even in the presence of hyponatraemia. The difficulty for clinicians is being able to accurately assess the ECF volume. However ADH may also be released in the face of a normal ECF volume, if there is an inadequate "effective" vascular volume:
Possible aids to identifying presence of an ECF deficit:
| Clinical history |
Ingestion of diuretics will lead to sodium loss in the urine. Other non-renal causes of sodium loss should be obvious eg diarrhoea. |
| Plasma K+ |
In the syndrome of inappropriate ADH secretion (SIADH), the plasma K+ is usually normal. If ECF volume low, plasma [K+] will be low secondary to hyperaldosteronism. This is exacerbated by the delivery of volume and bicarbonate to the cortical collecting duct eg. diuretics, vomiting. If plasma [K+] is high then aldosterone levels must be low.> |
| Plasma HCO3- |
In SIADH the plasma [HCO3-] is usually normal. In vomiting or diuretic-induced hyponatraemia, the plasma [HCO3-] is high, because of the associated metabolic alkalosis. Hyponatraemia of hypoaldosteronism is usually associated with a slightly low plasma [HCO3-]. |
| Plasma urea |
In SIADH the plasma urea level is low. This is the result of ECF volume expansion and increased urea
clearance. If there is a reduced "effective" circulating volume, there is a reduced GFR and therefore a reduced urea clearance and high plasma [urea]. |
| Plasma urate | In SIADH, the plasma urate concentration is reduced. |