Serum C-reactive Protein and Thioredoxin Levels in Subjects with Mildly Reduced Glomerular Filtration Rate

Shoko Tsuchikura; Tetsuo Shoji; Naoko Shimomura; Ryusuke Kakiya; Masanori Emoto; Hidenori Koyama; Eiji Ishimura; Masaaki Inaba; Yoshiki Nishizawa

Disclosures

BMC Nephrology. 2010;11:7 

In This Article

Background

Chronic kidney disease (CKD) is a newly recognized high-risk population for cardiovascular disease (CVD).[1] The relative risk of death from myocardial infarction is 10–30 times higher in hemodialysis patients (CKD stage 5D) as compared to the general population.[2] Atherosclerotic vascular changes are present in patients with CKD not yet treated with hemodialysis[3–5] as well as in hemodialysis patients.[6] The risk for CVD increases in a stepwise manner as glomerular filtration rate (GFR) declines.[7] The increased risk of CVD in reduced GFR may be explained at least partly by impairment of classical risk factors including hypertension,[8] dyslipidemia,[9] and glucose intolerance/insulin resistance.[10] In addition, inflammation and increased oxidative stress[11,12] presumably contribute to the CKD-related excess risk for CVD.[1]

Oxidative stress is determined by the balance between the production and elimination of reactive oxygen species (ROS).[13] Since superoxide anion and other ROS are difficult to be evaluated reliably in clinical conditions due to their very short half-lives, more stable markers have been measured in biological specimens. For example, oxidative modifications of lipids, proteins, and nucleic acids can be evaluated by thiobarbituric acids-reactive substances (TBARS),[14,15] advanced oxidation protein products (AOPP), and 8-hydroxydeoxyguanodine (8-OHdG),[16] respectively. In addition, proteins that are secreted into the circulation in response to oxidative stress may serve as the biomarkers for oxidative stress. Thioredoxin (TRX) is among such proteins. TRX is a 12 kD protein, secreted by most cell types, with a redox-active dithiol/disulfide in the active site consensus sequence: -Cys-Gly-Pro-Cys-,[17] showing anti-oxidative properties. Plasma TRX levels are increased in response to oxidative stress as shown in experimental[18] and human studies.[19–21] Also, serum TRX is known to be elevated in patients with increased oxidative stress, such as pancreatic cancer,[22] hepatitis C virus infection,[23] severe burn injury,[24] acquired immunodeficiency syndrome (AIDS),[25] rheumatoid arthritis,[26] heart failure,[27] steato hepatitis,[28] and interstitial lung disease.[29]

Uremia is considered as pro-oxidant state.[11,30] Previous studies demonstrated the elevated levels of biomarkers for oxidative modification of lipids[31] and proteins[15] in dialysis patients, and in advanced stages of CKD prior to renal replacement therapy.[32] So far, however, information is limited regarding possible changes in inflammation and oxidative stress among subjects with mild reduction of renal function.[33–35]

In the present study, we measured C-reactive protein (CRP) and TRX as biomarkers for inflammation and oxidative stress, and compared them between subjects with normal and mildly reduced glomerular filtration rate (GFR).

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