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      Plasma α-Oxoaldehyde Levels in Diabetic and Nondiabetic Chronic Kidney Disease Patients

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          alpha-Oxoaldehydes such as glyoxal (GO), methylglyoxal (MG), and 3-deoxyglucosone (3DG) are precursors of advanced glycation end products and exert direct toxicity to cells and tissues. Plasma levels of these substances are reportedly elevated in diabetes and dialysis patients, but the data on exact levels and clinical significance in chronic kidney disease (CKD) are limited. We evaluated plasma alpha-oxoaldehyde levels using liquid chromatography mass spectrometry methods in 19 healthy controls and 99 CKD patients with or without diabetes (n = 46 and n = 53, respectively). Mean plasma GO levels in control, CKD stage 1-2, CKD stage 3-5 and CKD stage 5D groups were 285 +/- 59, 339 +/- 88, 483 +/- 172 and 1,178 +/- 309 nM, respectively (p < 0.001). MG levels were 249 +/- 17, 265 +/- 27, 461 +/- 188 and 922 +/- 354 nM, respectively (p < 0.001). Moreover, significantly higher MG levels were observed in patients with cardiovascular disease history compared to those without. Plasma 3DG levels did not differ among CKD groups and were significantly higher in diabetic patients than in nondiabetic patients. Plasma GO and MG levels increase as the CKD stages progress and high plasma MG levels may be associated with an increased risk of CVD in CKD patients. Copyright 2008 S. Karger AG, Basel.

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          Most cited references 30

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          Chronic kidney disease as a risk factor for cardiovascular disease and all-cause mortality: a pooled analysis of community-based studies.

          Chronic kidney disease (CKD) is a major public health problem. Conflicting evidence exists among community-based studies as to whether CKD is an independent risk factor for adverse cardiovascular outcomes. After subjects with a baseline history of cardiovascular disease were excluded, data from four publicly available, community-based longitudinal studies were pooled: Atherosclerosis Risk in Communities Study, Cardiovascular Health Study, Framingham Heart Study, and Framingham Offspring Study. Serum creatinine levels were indirectly calibrated across studies. CKD was defined by a GFR between 15 and 60 ml/min per 1.73 m(2). A composite of myocardial infarction, fatal coronary heart disease, stroke, and death was the primary study outcome. Cox proportional hazards models were used to adjust for study, demographic variables, educational status, and other cardiovascular risk factors. The total population included 22,634 subjects; 18.4% of the population was black, and 7.4% had CKD. There were 3262 events. In adjusted analyses, CKD was an independent risk factor for the composite study outcome (hazard ratio [HR], 1.19; 95% confidence interval [CI], 1.07-1.32), and there was a significant interaction between kidney function and race. Black individuals with CKD had an adjusted HR of 1.76 (95% CI, 1.35-2.31), whereas whites had an adjusted HR of 1.13 (95% CI, 1.02-1.26). CKD is a risk factor for the composite outcome of all-cause mortality and cardiovascular disease in the general population and a more pronounced risk factor in blacks than in whites. It is hypothesized that this effect may be due to more frequent or more severe subclinical vascular disease secondary to hypertension or diabetes in black individuals.
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            Role of oxidative stress in diabetic complications: a new perspective on an old paradigm

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              Formation of glyoxal, methylglyoxal and 3-deoxyglucosone in the glycation of proteins by glucose.

              The glycation of proteins by glucose has been linked to the development of diabetic complications and other diseases. Early glycation is thought to involve the reaction of glucose with N-terminal and lysyl side chain amino groups to form Schiff's base and fructosamine adducts. The formation of the alpha-oxoaldehydes, glyoxal, methylglyoxal and 3-deoxyglucosone, in early glycation was investigated. Glucose (50 mM) degraded slowly at pH 7.4 and 37 degrees C to form glyoxal, methylglyoxal and 3-deoxyglucosone throughout a 3-week incubation period. Addition of t-BOC-lysine and human serum albumin increased the rate of formation of alpha-oxoaldehydes - except glyoxal and methylglyoxal concentrations were low with albumin, as expected from the high reactivity of glyoxal and methylglyoxal with arginine residues. The degradation of fructosyl-lysine also formed glyoxal, methylglyoxal and 3-deoxyglucosone. alpha-Oxoaldehyde formation was dependent on the concentration of phosphate buffer and availability of trace metal ions. This suggests that alpha-oxoaldehydes were formed in early glycation from the degradation of glucose and Schiff's base adduct. Since alpha-oxoaldehydes are important precursors of advanced glycation adducts, these adducts may be formed from early and advanced glycation processes. Short periods of hyperglycaemia, as occur in impaired glucose tolerance, may be sufficient to increase the concentrations of alpha-oxoaldehydes in vivo.

                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                October 2008
                12 June 2008
                : 28
                : 6
                : 871-878
                aResearch Division of Dialysis and Chronic Kidney Disease, Tohoku University Graduate School of Medicine, bDepartment of Blood Purification, Tohoku University Hospital and cNew Industry Creation Hatchery Center, Tohoku University, Sendai, Japan
                139653 Am J Nephrol 2008;28:871–878
                © 2008 S. Karger AG, Basel

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                Page count
                Pages: 8
                Original Report: Patient-Oriented, Translational Research


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