title: Role of lipid peroxidation, trace elements and anti-oxidant enzymes in chronic renal disease patients.
abstract: Plasma Selenium (Se), Zinc (Zn), Copper (Cu) and Aluminium (Al) levels, red blood cell vitamin E and antioxidant enzymes, glutathione peroxidase (GPX) and catalase activity were studied in 54 patients with renal diseases of different levels of kidney dysfunction. Group I (serum creatinine < 2 mg/dl), Group II (serum creatinine 2-4 mg/dl), Group III (serum creatinine 4.1-8 mg/dl), Group IV (serum creatinine 8.1-12 mg/dl) Group V (serum creatinine > 12 mg/dl); thirty two healthy subjects are controls. Plasma Zn (ug/L) and red blood cell vitamin E (ug/ml PRC) were decreased more significantly than controls (1348.59 +/- 43.72 vs 1318.89 +/- 45.62, and 3.38 +/- 0.45 vs 2.23 +/- 0.52) while plasma Selenium and Copper are within normal ranges. Plasma GSH-PX and catalase activity (IU/ml PRC) were also decreased (28.26 +/- 9.01 vs 20.48 +/- 6.79 and 7.54 +/- 1.91 vs 6.52 +/- 2.31) more significantly than controls. Lipid peroxidation products, plasma (umol/L) and urine malonaldehyde (MDA, umol/Ccr) were elevated (7.29 +/- 3.39 vs 92.94 +/- 61.66, and 32.08 +/- 24.60 vs 246.14 +/- 325.66) significantly (p < 0.0001). The lipid peroxidation abnormalities were seen in patients with normal renal function, which supports the role of oxidative stress early in the course of renal disease. Urine ammonia per GFR was also increased as well as urine B2m and NAG. There was no correlation between lipid peroxidation product (MDA) and any of the antioxidant enzymes, vitamin E, urine NH3, B2m, protein or NAG except urine ammonia and MDA per nephron which correlate with severity of kidney dysfunction which confirmed the role of complex processes in the progression of chronic renal failure. The early intervention to decrease oxygen consumption either by dietary protein restriction antioxidants such as vitamin E supplement or calcium channels blockers may be of value in preserving renal function in the setting of chronic renal failure.
authors.affiliation: Department of Medicine, Faculty of Medicine, Siriraj Hospital, Bangkok, Thailand.
authors.forename: L
authors.initials: L
authors.lastname: Ongajooth
authors.forename: S
authors.initials: S
authors.lastname: Ongajyooth
authors.forename: A
authors.initials: A
authors.lastname: Likidlilid
authors.forename: Y
authors.initials: Y
authors.lastname: Chantachum
authors.forename: C
authors.initials: C
authors.lastname: Shayakul
authors.forename: S
authors.initials: S
authors.lastname: Nilwarangkur
mesh_terms: D002908:Chronic Disease; D003404:Creatinine / Q000097:blood; D006801:Humans; D007674:Kidney Diseases / Q000097:blood / Q000503:physiopathology*; D015227:Lipid Peroxidation; D008315:Malondialdehyde / Q000032:analysis; D018384:Oxidative Stress; D014131:Trace Elements / Q000097:blood*
chemical_list: D014131:Trace Elements; D008315:Malondialdehyde; D003404:Creatinine