Taccone-Gallucci M, Lubrano R, Belli A, Meloni C, Morosetti M, Meschini L, Elli M, Boffo V, Pisani F, Giardini O
Clinica Chirurgica, Dipartimento di Chirurgia, II Universitá di Roma, Italy.
ASAIO Trans. 1989 Jul-Sep;35(3):533-5. doi: 10.1097/00002480-198907000-00116.
Hemodialysis patients display increased oxidative damage to red blood cell (RBC) membranes, characterized by elevated levels of malonyldialdehyde (MDA), a short chain aldehyde produced by the oxidation of the polyunsaturated fatty acids (PUFA) in the RBC membranes. This is the result of a metabolic blockage of the pentose-phosphate shunt in uremic patients, which causes reduced detoxification of highly oxidative free radicals. The oxidative damage induces increased RBC rigidity and decreased RBC deformability, therefore favoring hemolysis. The aim of this work was to determine if a functioning renal graft would restore normal erythrocyte metabolism, reducing the oxidative damage. To this end, we have determined RBC MDA concentrations in 20 hemodialysis (HD) patients (RBC MDA 18.22 +/- 4.36 micrograms/ml packed RBC), 20 renal transplant (T) patients with well functioning grafts (serum creatinine less than 2 mg%) (RBC MDA 1.2 +/- 0.4 micrograms/ml packed RBC) (T vs. HD P less than 0.005) and 20 healthy controls (HC) (RBC MDA 1.44 +/- 0.6 micrograms/ml packed RBC) (HC vs. HD P less than 0.005; HC vs. T NS). Our findings show that a well-functioning renal graft restores normal RBC metabolism and eliminates the oxidative damage induced by uremia.
血液透析患者的红细胞（RBC）膜显示出氧化损伤增加，其特征是丙二醛（MDA）水平升高，MDA是一种由红细胞膜中多不饱和脂肪酸（PUFA）氧化产生的短链醛。这是尿毒症患者磷酸戊糖旁路代谢受阻的结果，该受阻导致高氧化性自由基的解毒作用降低。氧化损伤导致红细胞刚性增加和变形性降低，从而促进溶血。这项工作的目的是确定一个功能正常的肾移植是否会恢复正常的红细胞代谢，减少氧化损伤。为此，我们测定了20名血液透析（HD）患者（每毫升压积红细胞中RBC MDA为18.22±4.36微克）、20名肾移植（T）且移植肾功能良好（血清肌酐低于2mg%）的患者（每毫升压积红细胞中RBC MDA为1.2±0.4微克）（T组与HD组比较，P<0.005）以及20名健康对照者（HC）（每毫升压积红细胞中RBC MDA为1.44±0.6微克）（HC组与HD组比较，P<0.005；HC组与T组比较，无显著性差异）的RBC MDA浓度。我们的研究结果表明，一个功能良好的肾移植可恢复正常的RBC代谢，并消除尿毒症诱导的氧化损伤。
