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  • Title: [Malondialdehyde and selected antioxidant plasma levels in conservatively treated patients with kidney diseases].
    Author: Gazdikova K, Gvozdjakova A, Kucharska J, Spustova V, Braunova Z, Dzurik R.
    Journal: Bratisl Lek Listy; 2000; 101(9):490-4. PubMed ID: 11187051.
    Abstract:
    UNLABELLED: Oxidation stress and decreased antioxidative capacity participate in the progression and complications of renal diseases such as hyperlipoproteinemia or cardiovascular diseases. Many data have been collected on oxidation stress in dialysed patients, however a shortage of information is evident in conservatively treated patients. STUDY AIMS: To determine the blood and/or plasma levels of MDA and the selected antioxidants, i.e. Coenzyme Q10 (CoQ), alpha-tocoferol, beta-carotene in conservatively treated patients with kidney diseases. PATIENTS AND METHODS: Fifty five patients (45 with interstitial nephritis and 10 with glomerulonephritis) were included. They were divided into 3 subgroups on the basis of their clearance of creatinine (Ckr). Only validated methods have been exploited for the determination of variables. RESULTS: MDA plasma levels were increased (5.37 +/- 0.10, reference range (rr.) < 4.5 mumol/l) with the highest levels in patients treated by immunosuppression. CoQ plasma (0.35 +/- 0.04, rr. 0.4-1.0 mumol/l) and blood (0.30 +/- 0.03 mol/l) were decreased, notably in patients with interstitial nephritis. No correlation with Ckr was apparent. alpha-tocopherol plasma levels (42.1 +/- 3.04, rr. 15-40 mumol/l) were increased, but the concentrations increased further with the decreasing kidney function. beta-carotene plasma (2.14 +/- 0.39, rr. > 0.8 mumol/l) were in reference range but decreased with the decrease of kidney function. CONCLUSIONS: CoQ plasma levels are decreased and MDA levels increased in conservatively treated kidney disease patients even in just slightly decreased renal function. beta-carotene levels decrease only in advanced renal failure. These changes could participate in kidney disease progression and it is suggested that their correction opens the possibility of progression inhibition. (Tab. 3, Ref. 27.)
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