Abstract
We detected increased concentrations of lipoperoxidation products, as malondialdehyde, in the serum of an infant with classic hemolytic-uremic syndrome. The concentrations declined when peritoneal dialysis was initiated and eventually returned to normal after clinical recovery. Our observation adds to the existing body of evidence that links the pathogenesis of hemolytic-uremic syndrome to peroxidative damage and to the rationale for using antioxidant agents as part of the therapy for this disease process.
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