Urine electrolytes in metabolic alkalosis

No time like the present for a quick review of urine electrolytes. Is there any such thing as a ‘normal’ urine sodium? Not really – like all great answers in medicine, ‘it depends’. In general, in patients who are euvolaemic, the urine sodium excretion will directly correlate with the degree of dietary sodium ingestion.

In the setting of effective volume depletion, neurohormonal activation results in stimulation of a number of compensatory mechanisms (RAAS, non-osmotic ADH release, baroreceptor activation, to name a few). These systems are charged with the task of preserving blood pressure and perfusion to vital organs – sodium retention by the kidney is one of the major players in achieving this.

Therefore, a low spot urine sodium (e.g. less than 20 mmol/L) is often viewed as being consistent with a sodium avid state, be that appropriate (e.g. shock) or not (e.g. decompensated heart failure).

In certain situations the urine sodium cannot be interpreted this way. The major condition I’m thinking of is metabolic alkalosis. In this setting, the filtered bicarbonate load increases and overwhelms the tubular reabsorptive capacity, resulting in bicarbonaturia and urine pH over 6.5. In order to maintain a degree of electroneutrality, a corresponding cation must travel along with it. Sodium fulfils this requirement, thereby making the urine sodium concentration necessarily high and not reflective of the patient’s volume status, as long as bicarbonaturia persists.

In this setting, the urine chloride is a better measurement of volume status, with a low urine chloride (in metabolic alkalosis) more suggestive of a hypovolaemic state. Furthermore, hypochloraemia contributes to the maintenance of a metabolic alkalosis, giving another reason for the kidney to try to hold onto as much chloride as possible.

See Viresh’s blog and Ernest’s blog for more discussion on urine sodium and metabolic alkalosis.