Cerebral edema after rapid dialysis is not caused by an increase in brain organic osmolytes.

Abstract

Dialysis disequilibrium syndrome (DDS) is characterized by the neurologic deterioration and cerebral edema that occurs after hemodialysis. To investigate the pathogenesis of DDS, the effects of rapid hemodialysis on brain electrolytes, urea, and several organic osmolytes were studied in the rat. Forty-two h after bilateral ureteral ligation, 11 uremic rats were hemodialyzed for 90 min, yielding a decrease in plasma urea from 96 +/- 4 to 44 +/- 5 mM (p < 0.01). This group was compared with 10 uremic and 11 nonuremic animals that were not dialyzed. In dialyzed animals, compared with nondialyzed uremic controls, there was an increase in brain water (3.98 +/- 0.02 versus 3.77 +/- 0.02 L/kg dry wt; P < 0.01) and the brain to plasma (urea) ratio (1.32 versus 0.65). There was no significant difference in the brain content of sodium and potassium between groups. The retention of brain urea, despite the large decrease in plasma urea concentration, was able to account for the increase in brain water observed in rapidly dialyzed animals. Major organic osmolytes in the brain, including glutamine, glutamate, taurine and myoinositol, did not increase significantly after rapid dialysis. Cerebral edema in this model of DDS was primarily due to a large brain-to-plasma urea gradient, not to the formation of organic osmolytes.