Oxidative damage of erythrocyte membrane in nephrotic syndrome

Abstract

Erythrocytes are target cells for peroxidative damage. Abnormal susceptibility of erythrocyte lipids to peroxidation is believed to reflect a similar abnormality in other organs and tissues. The changes in erythrocyte lipid peroxidation [measured by malonyldialdehyde (MDA) concentration] and erythrocyte membrane cholesterol (EMC) and their correlation with plasma lipid changes were studied in 36 children with steroid-responsive minimal change nephrotic syndrome (MCNS) (16 in relapse, 20 in remission) and 30 matched healthy controls. Erythrocyte MDA levels were significantly higher in relapse [126.3+/-40.6 nmol/g hemoglobin (Hb)] compared with remission (101.2+/-21.3 nmol/g Hb, P<0.02) and in controls (95.4+/-20.4 nmol/g Hb, P<0.001). Plasma MDA levels in relapse were also higher than in remission (4.26+/-1.19 nmol/ml vs. 3.16+/-1.18 nmol/ml, P<0.01), and in controls (2.49+/-0.86 nmol/ml, P<0.001). The EMC content changed significantly during remission (1.22+/-0.15 mg/10(10) cells in relapse, 1.09+/-0.19 mg/10(10) cells in remission, P<0.04). These results show an increased sensitivity of red cells to lipid peroxidation in patients with steroid-sensitive nephrotic syndrome without the development of renal failure and anemia. Lipid peroxidation of plasma lipids and erythrocyte membrane may be a primary phenomenon, but this should be confirmed by investigation of peroxidation of renal lipids.

Anti‐oxidant status in relation to lipoproteins, leptin and pro‐inflammatory cytokines in children with steroid‐sensitive nephrotic syndrome

“…In previous studies, plasma or erythrocyte MDA increased and whole‐blood GSH decreased in nephrotic children compared with remission and healthy controls 16,24 . In the study by Fydryk et al ., 6 increased plasma MDH and enhanced SOD activity were found in relapse patients.…”

“…Although, in general, SSNS is not a progressive nephropathy and responds well to steroids other forms of NS, including focal segmental glomerulosclerosis and membranoproliferative glomerulonephritis, are usually steroid resistant and progressive nephropathies 1 . An increase in peroxidation of lipids and lipoproteins may cause the release of free radicals, cytokines and growth factors that could result in glomerular injury 16 . A change in glomerular filtration barrier integrity, resulting in proteinuria, may affect the structure of the glomerular capillary wall, its function or both 17 .…”

Etiology and management of dyslipidemia in children with chronic kidney disease and end-stage renal disease

“…Active NS results in significant proteinuria and hyperlipidemia, the latter featuring elevated TC with or without elevated TG [51,52]. Specifically, patients with NS exhibit elevated levels of all Apo-B containing lipoproteins, due to reduced catabolism, including VLDL, IDL, LDL-C, and Lp(a); conversely, HDL-C levels are usually normal [53][54][55][56][57]. The pathogenesis includes increased production together with reduced clearance of lipoproteins [54,[58][59][60][61][62][63].…”

Increase in liver antioxidant enzyme activities in non‐alcoholic fatty liver disease

“…Erythrocytes, which are potential target cells for peroxidative damage, exhibit oxidative stress in patients with nephrotic syndrome (29) and with type 1 diabetes (30). The unusually high susceptibility of erythrocyte lipids to peroxidation is thought to reflect similar abnormalities in organs and tissues including the liver.…”