Listeria brain abscess in an immunosuppressed child

Abstract

speculate that the marked elevations serum uric acid which occur in Reye syndrome are capable of inducing acute renal failure, particularly in patients with lactic acidosis.: It is known that uric acid and lactic acid compete for the same renal excretory mechanism, ~ and a marked increase of plasma ~aric acid would, therefore, be expected with lactic acidemia. Although we did not measure lactic acid levels in our patient, the serum anion gap [Na-(C1 + COO] on admission and prior to correction was markedly elevated. In the absence of ketosis, this probably reflects lactic acidemia. T'he glomernli and tubules in uric acid nephropathy may appear entirely normal, as in our patient or show ischemic as shown by others reporting renal insufficiency associated with hepatic dysfunction.:' Renal ultrastructure in our patient (Fig. 2) demonstrated enlarged vacuoles, probably related to the cellular lysosome system, filled with membranous and floccular debris and compatible with changes found secondary to mannitol infusions.' We did not observe fatty infiltration. The renal mitochondria were not swollen or disrupted. -Iqae renal biopsy was performed one week after the diagnostic liver biopsy when the patient was in the early recovery phase of acute renal failure. Although renal failure may aggravate the clinical course of patients with acute encephalopathy and hepatic dysfunction, the prognosis appears to be determined by the encephalopathy rather than the renal failure.' :' Our