URIC-ACID, ANION GAP AND UREA CONCENTRATION IN THE DIAGNOSTIC-APPROACH TO HYPONATREMIA

We analyzed the serum anion gap (AG = sodium plus potassium minus chlo ride plus bicarbonate, N = 11-21 mEq/l), serum uric acid and urea conc entrations in hyponatremia of various origins. We found that character istic chemical patterns emerged in association with different hypotoni c states: Low uric acid concentration was typically observed in the SI ADH and in hyponatremia related to hypopituitarism. The same observati on was also frequently noted in hyponatremia secondary to diuretics or to polydypsia. In the SIADH, we observed a decrease in the AG but to a greater extent (-26%) than one would expect from the simple dilution al effect (-16%). Fifty percent of the patients presented an AG lower than 11 mEq/l. In patients with diuretic-related hyponatremia, one gro up presented an hypouricemia and a low AG as in SIADH (reflecting volu me expansion), in the other group the AG was normal or increased as wa s uric acid concentration (reflecting volume depletion). In adrenocort icotropin deficiency, hyponatremia was typically associated with a low bicarbonate concentration, a normal AG and hypouricemia. In polydypsi c patients with hyponatremia, the AG was usually normal or increased d espite sometimes very low sodium levels. Uric acid levels were highly variable, most often decreased. We also noted in these patients that t he serum urea levels were correlated with urine osmolality (R = +0.8; p <0.001), and in 40% of them we observed very low blood urea concentr ation (0.5-2 mmol/l) at the admission time. In hyponatremia related to cardiac failure or cirrhosis, the AG was usually normal despite mild hypoproteinemia.