An experimental model of canine normothermic renal ischemia was used to determine whether lysosomal urinary enzyme excretion reflects the extent of ischemic cellular injury, as assessed by subsequent renal function (serum creatinine level) and morphologic changes. The value of a lysosomal membrane-stabilizing agent (methylprednisolone) in protecting kidneys from ischemic damage by preventing lysosomal enzyme release was assessed. Results showed conclusively that urinary enzyme activities of beta-galactosidase and N-acetyl-beta-glucosaminidase are valuable indicators of renal cellular damage and functional outcome after ischemic injury, and that methylprednisolone at a dose of 30 mg/kg, given intravenously 1 hour before a 1-hour period of normothermic ischemia, protects the kidney both biologically and morphologically, by reducing the excretion of lysosomal enzymes after revascularization.
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