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      Tumor Necrosis Factor (TNF-α) and C-reactive Protein (CRP) are Positively Associated with the Risk of Chronic Kidney Disease in Patients with Type 2 Diabetes

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          Abstract

          Purpose

          Chronic low-grade inflammation may induce chronic kidney disease in patients with type 2 diabetes. This study investigated the relation between inflammatory biomarkers and chronic kidney disease in patients with type 2 diabetes, which has not yet been reported in Asian populations.

          Materials and Methods

          A cross-sectional study was performed in 543 patients recruited from diabetic clinics for an ongoing, prospective study. Multivariate logistic regression was used to evaluate the association between inflammatory biomarkers and the presence of chronic kidney disease (estimated glomerular filtration rate < 60 mL/min per 1.73 m 2 by the simplified Modification of Diet in Renal Disease equation using plasma creatinine).

          Results

          The risk of chronic kidney disease increased in the highest quartiles of C-reactive protein (CRP) [multivariate odds ratio (OR) = 3.73; 95% CI = 1.19-1.70] and tumor necrosis factor-α (multivariate OR = 4.45; 95% CI = 1.63-12.11) compared to the lowest quartiles after adjustments for age, sex, zinc intake, and other putative risk factors for chronic kidney disease.

          Conclusion

          Our results suggest that CRP and tumor necrosis factor-α may be independent risk factors for chronic kidney disease in patients with type 2 diabetes. A causal mechanism of this association should be evaluated in a follow-up study of Korean patients with type 2 diabetes.

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          Elevations of inflammatory and procoagulant biomarkers in elderly persons with renal insufficiency.

          Anthony J Bleyer, Casey Crump, Linda F. Fried … (2003)
          Renal insufficiency has been associated with cardiovascular disease events and mortality in several prospective studies, but the mechanisms for the elevated risk are not clear. Little is known about the association of renal insufficiency with inflammatory and procoagulant markers, which are potential mediators for the cardiovascular risk of kidney disease. The cross-sectional association of renal insufficiency with 8 inflammatory and procoagulant factors was evaluated using baseline data from the Cardiovascular Health Study, a population-based cohort study of 5888 subjects aged > or =65 years. C-reactive protein, fibrinogen, factor VIIc, and factor VIIIc levels were measured in nearly all participants; interleukin-6, intercellular adhesion molecule-1, plasmin-antiplasmin complex, and D-dimer levels were measured in nearly half of participants. Renal insufficiency was defined as a serum creatinine level > or =1.3 mg/dL in women and > or =1.5 mg/dL in men. Multivariate linear regression was used to compare adjusted mean levels of each biomarker in persons with and without renal insufficiency after adjustment for other baseline characteristics. Renal insufficiency was present in 647 (11%) of Cardiovascular Health Study participants. After adjustment for baseline differences, levels of C-reactive protein, fibrinogen, interleukin-6, factor VIIc, factor VIIIc, plasmin-antiplasmin complex, and D-dimer were significantly greater among persons with renal insufficiency (P<0.001). In participants with clinical, subclinical, and no cardiovascular disease at baseline, the positive associations of renal insufficiency with these inflammatory and procoagulant markers were similar. Renal insufficiency was independently associated with elevations in inflammatory and procoagulant biomarkers. These pathways may be important mediators leading to the increased cardiovascular risk of persons with kidney disease.
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            Dietary Reference Intakes for Koreans

            (2010)
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              Acute-phase markers of inflammation and glomerular structure in patients with type 2 diabetes.

              M Bruseghin, Alois Saller, Michele Dalla Vestra … (2005)
              Type 2 diabetes is frequently associated with an inflammatory status; the relationships between low-grade inflammation and diabetic nephropathy are still unclear. The aim of this study was to evaluate the relationships between acute-phase markers of inflammation, glomerular structure, and albumin excretion rate (AER) in type 2 diabetes. In 74 patients with type 2 diabetes (23 normoalbuminuric, 30 microalbuminuric, and 21 proteinuric) fibrinogen, serum amyloid A protein (SAA), C-reactive protein (CRP), and IL-6 were determined. AER was measured on three 24-h urine collections; GFR was measured by 51Cr EDTA plasma clearance. A kidney biopsy was performed, and mesangial fractional volume [Vv(mes/glom)] and glomerular basement membrane (GBM) width were estimated by electron microscopic morphometric analysis. CRP, fibrinogen, SAA, and IL-6 differed among groups, with proteinuric patients having the highest levels. SAA and fibrinogen correlated with AER (P 396 nm), CRP, SAA, and IL-6 were higher than in patients with normal GBM width (P < 0.003, P < 0.004, and P < 0.0004, respectively). GBM width was directly correlated with fibrinogen (r = 0.33, P < 0.002) and IL-6 (r = 0.25 P < 0.05). In conclusion, this study demonstrates that acute-phase markers of inflammation are associated with nephropathy status and GBM thickening, suggesting a role for inflammation in the pathogenesis of diabetic glomerulopathy.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Yonsei Med J
                Journal ID (publisher-id): YMJ
                Title: Yonsei Medical Journal
                Publisher: Yonsei University College of Medicine
                ISSN (Print): 0513-5796
                ISSN (Electronic): 1976-2437
                Publication date (Print): 01 July 2010
                Publication date (Electronic): 24 May 2010
                Volume: 51
                Issue: 4
                Pages: 519-525
                Affiliations
                [1 ]Department of Nutritional Science and Food Management, Ewha Womans University, Seoul, Korea.
                [2 ]Huh's Diabetes Clinic & the 21C Diabetes and Vascular Research Institute, Seoul, Korea.
                Author notes
                Corresponding author: Dr. Kap Bum Huh, Huh's Diabetes Clinic & the 21C Diabetes and Vascular Research Institute, 40-9 Nogosan-Dong, Mapo-Gu, Seoul 121-806, Korea. Tel: 82-2-718-1827, Fax: 82-2-704-5750, huh7181827@ 123456hanmail.net and Dr. Wha Young Kim, Department of Nutritional Science and Food Management, Ewha Womans University, 11-1 Daehyeon-dong, Seodaemun-gu, Seoul 120-750, Korea. Tel: 82-2-3277-3093, Fax: 82-2-3277-3103, wykim@ 123456ewha.ac.kr

                *These authors contributed equally to this work.

                Article
                DOI: 10.3349/ymj.2010.51.4.519
                PMC ID: 2880263
                PubMed ID: 20499416
                SO-VID: 5e333b1c-f563-4460-bdc5-52529f012012
                Copyright © © Copyright: Yonsei University College of Medicine 2010
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 05 August 2009
                Date revision received : 17 September 2009
                Date accepted : 17 September 2009
                Categories
                Subject: Original Article
                Subject: Endocrinology & Metabolism

                ScienceOpen disciplines: Medicine
                Keywords: type 2 diabetes,chronic kidney disease,c-reactive protein,inflammation,tumor necrosis factor-α
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: type 2 diabetes, chronic kidney disease, c-reactive protein, inflammation, tumor necrosis factor-α

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