Plasma and tissue levels of free oxygen radicals in recipients of kidneys from non–heart-beating donors: does recipient pretreatment with antioxidant drugs make sense? An experimental study in pigs

Abstract

THE SHORTAGE of kidneys for transplantation and the growing waiting list of patients with end-stage renal disease (ESRD) has led transplant physicians to expand the criteria for kidney donation while trying to maintain good posttransplant graft function. Kidneys from non–heart-beating donors (NHBD) represent a possible solution to this problem. Unfortunately, these kidneys have a high rate of delayed graft function (DGF) and primary nonfunction (PNF) compared to organs procured from heart-beating donors. The main cause of the poorer results is warm ischemia time (WIT), which significant by damages kidneys from NHBD with ischemia–reperfusion syndrome (IRS). Free oxygen radicals (FORs), which originate in a temporarily ischemic graft after reperfusion, are harmful to transplanted kidneys; their increased production leads to lipid peroxidation and formation of malondialdehyde (MDA). This damage is greater in ESRD patients who have a depressed intracellular antioxidant defense, as manifested by decreased activities of superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) in erythrocytes. The concentration of the main intracellular antioxidant—glutathione (GSH)—is also depressed. Although current preservation solutions contain various antioxidants, they are still designed for kidney retrieval from heart-beating donors, where the intensity of the IRS is lower than that after transplantation from NHBD. The exogenous application of antioxidants to patients who are on the waiting list for kidney transplantation may have an important protective effect on kidney damage from IRS. The aim of our experimental study was to evaluate the effects on plasma and tissue concentrations of FORs of administration of a multivitamin supplemented with trace elements and ascorbic acid to recipients of kidneys from NHBD.