Urease and the acidosis of urinary intestinal diversion.

Previous investigators have suggested that urinary tract infections with urea-splitting organisms may be a primary etiologic factor in the acidosis which is seen after urinary diversion. This study employs a model in which small intestinal segments are perfused with an artificial urine solution over a three hour period. Urease is then added in order to determine its effect on acid-base balance and net intestinal electrolyte transport. Urease created no significant increase in acid load (delta HCO3- = -7.5 +/- 2.2 for controls vs. -8.7 +/- 2.9 for urease group), but did increase the osmolality of the intestinal contents and resulted in a 24% increase in free water loss (p = .037). Analysis of sodium and chloride movement following the addition of urease to the perfusate suggests that both ammonium and bicarbonate are absorbed by the intestinal segment. Thus any acidosis resulting from increased ammonium absorption following the addition of urease appears to be offset by concomitant bicarbonate absorption. The azotemia of urinary diversion appears to be primarily the result of urea absorption, partially the result of ammonium absorption, and is not significantly increased by urease.