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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE  
Year : 2012  |  Volume : 23  |  Issue : 2  |  Page : 286-289
Evaluation of high sensitivity creactive protein and glycated hemoglobin levels in diabetic nephropathy


1 Department of Physiology, M. S. Ramaiah Medical College, Bangalore, India
2 Department of Biochemistry, M. S. Ramaiah Medical College, Bangalore, India
3 Department of Biochemistry, Sapthagiri Institute of Medical Sciences and Research Centre, Bangalore, India
4 Department of Nephrology, M. S. Ramaiah Medical College, Bangalore, India
5 Department of Endocrinology, M. S. Ramaiah Medical College, Bangalore, India

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Date of Web Publication28-Feb-2012
 

   Abstract 

Diabetic nephropathy (DN) is one of the major long-term complications of diabetes mellitus (DM). Type 2 DM is frequently associated with an inflammatory status, but limited information is available on the relationship between low-grade inflammation and DN. The aim of the study is to determine the serum level of high sensitivity C-reactive protein (hsCRP) in DN patients and to compare with that of normal subjects and to study the association between serum hsCRP levels and glycated hemoglobin (HbA1c) levels. Fifty DN patients in the age group of 50- 60 years with more than ten years of duration of diabetes were recruited for this study and 25 age-and sex-matched healthy subjects were included in this study as controls. Serum hsCRP levels were measured by turbidometry method. There was a statistically significant increase in serum hsCRP levels in DN cases as compared to normal controls. The hsCRP levels showed a positive correlation with HbA1c in DN. These results suggest that estimation of serum hsCRP levels and aiming at good glycemic control help in early intervention and prevention of further com­plications in diabetic patients.

How to cite this article:
Roopakala M S, Pawan H R, Krishnamurthy U, Wilma Delphine Silvia C R, Eshwarappa M, Prasanna Kumar K M. Evaluation of high sensitivity creactive protein and glycated hemoglobin levels in diabetic nephropathy. Saudi J Kidney Dis Transpl 2012;23:286-9

How to cite this URL:
Roopakala M S, Pawan H R, Krishnamurthy U, Wilma Delphine Silvia C R, Eshwarappa M, Prasanna Kumar K M. Evaluation of high sensitivity creactive protein and glycated hemoglobin levels in diabetic nephropathy. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2014 Dec 25];23:286-9. Available from: http://www.sjkdt.org/text.asp?2012/23/2/286/93155

   Introduction Top


Diabetic nephropathy (DN) is a progressive kidney disease caused by angiopathy of capil­laries in glomeruli secondary to longstanding diabetes and is the major cause of morbidity and mortality in patients with Type 2 diabetes mellitus (DM). This emphasizes the impor­tance of interventions that help patients with Type 2 diabetes to reduce the risk of nephro-pathy. Previous studies have proved that Type 2 DM is frequently associated with chronic inflammatory state. [1],[2] Chronic inflammation plays an important role in the development and progression of late complications of diabetes. [3],[4] C-reactive protein (CRP), an acute phase re-actant, is a highly sensitive marker of inflam­mation. Its level rises dramatically during an inflammatory processes. [5] CRP has a long half life, affordability of estimation, and stability of its levels with no circadian variation, and therefore is one of the best markers of vascular inflammation. [6] CRP has been found to be associated with disorders like DM, cardiovas­cular disorders, metabolic syndrome, renal failure, etc. [2],[7],[8] Serum high sensitivity CRP (hsCRP) level is higher in patients with Type 2 diabetes than in normal subjects and plays an important role in the development and pro­gression of Type 2 DM. [9] It is also shown that the level of this marker of inflammation cor­relates with the levels of glycemic control, such as glycated hemoglobin A 1c (HbA 1c ). [10] But limited information is available on the relationship between low-grade inflammation and DN. Therefore, the present study was undertaken to evaluate serum hsCRP levels in DN.


   Materials and Methods Top


Fifty clinically diagnosed DN patients in the age group of 50-65 years with more than ten years of duration of Type II DM, on conser­vative management, attending the outpatient departments of Endocrinology and Nephrology of M.S. Ramaiah Memorial Hospital, Bangalore, were included in the study group. Twenty-five age- and sex-matched healthy subjects cons­tituted the control group. All the subjects completed a standard questionnaire regarding current medication and duration of diabetes. Subjects with history of any significant in­fections, trauma, malignancy, smoking, cancer, rheumatoid arthritis, those on any anti-infla­mmatory drug or with body mass index (BMI) >30 were excluded from the study. Patients on dialysis were also excluded. This study was approved by the institution's ethics committee, and informed consent was obtained from every subject. After 12 hours of fasting, blood samples were collected under aseptic precautions from me­dian cubital vein using commercially available vacutainers. The level of HbA1c was deter­mined by borate affinity assay (NycoCard, AXIS-SHIELD PoC AS, Norway). Serum creatinine was estimated by Modified Jaffe's method [11] using an autoanalyzer. Serum hsCRP concentration was measured by using a latex-enhanced immune-nephelometer (Biosystems, Barcelona, Spain).


   Statistical Analysis Top


Analysis was done by using the statistical software SPSS 11.0 and Systat 8.0. The thres­hold of statistical significance was defined as P < 0.05. Pearson's correlation coefficient was used to find the relationship between hsCRP and HbA1c.


   Results Top


The levels of serum creatinine, hsCRP, and glycated hemoglobin were higher than normal in the study group. Compared with the control group, these values were significantly higher in the study group (P < 0.001) [Table 1]. There was a statistically significant positive correla­tion between hsCRP and glycated hemoglobin in DN patients [Table 2]. In healthy controls, hsCRP showed no significant correlation with any of the parameters [Table 3].
Table 1: Comparison of measured parameters in healthy controls and diabetic nephropathy cases.

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Table 2: Correlation of serum creatinine, HbA1c, and hsCRP in diabetic nephropathy.

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Table 3: Correlation of serum creatinine HbA1c and hsCRP in controls.

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   Discussion Top


In this study, the mean values of serum hsCRP levels were significantly elevated in DN patients when compared with healthy con­trols (P < 0.001). The results indicate the pre­sence of inflammatory process in DN. Therefore, inflammation reflects the severity of the disease and signifies the presence of ongoing disease process. These observations are consistent with previous studies. [3],[12]

There are several possible mechanisms by which chronic low-degree inflammation might be induced in diabetes and its complications. In a hyperglycemic condition, the concentra­tion of advanced glycation end products in­creases. Advanced glycation end products have been shown to activate macrophages, increase oxidative stress, and upregulate the synthesis of interleukin-1, interleukin-6 (IL-6), and tu­mor necrosis factor, resulting in the production of CRP. [13] Another possibility is that increase in CRP concentrations is related to adipose tissue derived cytokines. [14] However, the role of adipose tissue as a possible cause of the chronic inflammatory condition in patients with DN requires further investigation.

There was a statistically significant positive correlation of serum hsCRP levels with HbA1c indicating the role of poor glycemic control in the development of nephropathy. Studies have shown similar association between hyper-glycemia and inflammation. [15] It is known that glycation triggers the inflammatory process, leading to a rise in hsCRP levels. Thus, hsCRP can predict the onset of glycation-induced in­flammatory process secondary to poor gly-cemic control. [3] It may not be just the burden of glucose exposure (long duration of diabetes) but also decreased insulin sensitivity plays a vital role, and they have a common denomi­nator, low-grade inflammation; therefore, poor glycemic control along with decreased insulin sensitivity probably act in concert in the patho-genesis of DN. Low-grade inflammation may be a risk factor for the nephropathy in patients with type-2 diabetes. To evaluate this possi­bility, prospective studies are required. The limitation of the study was including nor-motensive healthy controls instead of patients with microalbuminuria and on angiotensin converting enzyme (ACE) inhibitors because ACE inhibitors inhibit the expression of pro-inflammatory cytokines such as IL-6, which suggests that some of the beneficial effects of ACE inhibitors could at least in part be me­diated via pro-inflammatory genes.[16] From this study we conclude that there is a progressive increase in hsCRP levels in DN patients. The low-grade inflammation, indicated by hs-CRP, and hyperglycemia, indicated by HbA1c, together contribute to the pathoge-nesis of DN. Therefore, inflammation reflects the severity of the disease and signifies the presence of ongoing disease process. We also found a positive correlation between serum levels of hsCRP and HbA1c in DN patients. Thus, aiming at good glycemic control and estimation of serum hsCRP levels will pos­sibly be of help in planning early intervention, thereby preventing further complications which in turn may help preserve renal function in DN patients.

 
   References Top

1.Pfützner A, Standl E, Strotmann HJ, et al. Association of high-sensitive C-reactive pro­tein with advanced stage beta-cell dysfunction and insulin resistance in patients with type 2 diabetes mellitus. Clin Chem Lab Med 2006; 44(5):556-60.  Back to cited text no. 1
    
2.Aronson D. Hyperglycemia and the patho-biology of diabetic complications. Adv Cardiol 2008;45:1-16.  Back to cited text no. 2
    
3.Schalkwijk CG, Poland DC, Van Dijk W, et al. Plasma concentration of C-reactive protein is increased in Type I diabetic patients without clinical macroangiopathy and correlates with markers of endothelial dysfunction: evidence for chronic inflammation. Diabetologia 1999; 42:351-7.  Back to cited text no. 3
    
4.Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease. Circulation 1998; 97:425-8.  Back to cited text no. 4
    
5.Dong Q, Wright JR. Expression of C-reactive protein by alveolar macrophages. J Immunol 1996;56:4815-20.  Back to cited text no. 5
    
6.Wang AY. Prognostic value of C-reactive protein for heart disease in dialysis patients.Curr Opin Invest Drugs 2005;6:879-86.  Back to cited text no. 6
    
7.Doggen CJ, Berckmans RJ, Sturk A, Cats VM, Rosendaal FR. C-reactive protein, cardiovascular risk factors and the association with myo­cardial infarction in men. J Intern Med 2000; 248:406-14.  Back to cited text no. 7
    
8.Kang ES, Kim HJ, Ahn CW, et al. Rela­tionship of serum high sensitivity C-reactive protein to metabolic syndrome and micro­vascular complications in type 2 diabetes. Diabetes Res Clin Pract 2005;69:151-9.  Back to cited text no. 8
    
9.Li CZ, Xue YM, Gao F, Wang M. Deter­mination of serum highly sensitive C-reactive protein in patients with type 2 diabetes. Di Yi Jun Yi Da Xue Xue Bao 2004;24(7):791-3.  Back to cited text no. 9
    
10.Kalousová M, Zima T, Tesar V, Sulková S, Fialová L. Relationship between advanced gly-coxidation end products, inflammatory mar­kers/acute-phase reactants, and some auto­antibodies in chronic hemodialysis patients. Kidney Int 2003;63:S62-4.  Back to cited text no. 10
    
11.Bartels H, Böhmer M. Micro-determination of creatinine. Clin Chim Acta 1971;32(1): 81-5.  Back to cited text no. 11
    
12.Romao JE, Haiashi AR, Elias RM, et al. Positive acute-phase inflammatory markers in different stages of chronic kidney disesase. Am J Nephrol 2006;26:59-66.  Back to cited text no. 12
    
13.Yan SF, Ramasamy R, Naka Y, Schmidt AM. Glycation, Inflammation, and RAGE. A Sca­ffold for the Macrovascular Complications of Diabetes and Beyond. Circ Res 2003;93:1159-69.  Back to cited text no. 13
    
14.Alexandraki K, Piperi C, Kalofoutis C, Alaveras A, Kalofoutis A. Inflammatory process in type 2 diabetes: The role of cytokines. Ann N Y Acad Sci 2006;1084:89-117.  Back to cited text no. 14
    
15.Rekeneire DN, Peila R, Ding J, et al. Diabetes, hyperglycemia, and inflammation in older Individuals. The Health, Aging and Body Com­position study. Diabetes Care 2006;29:1902-8.  Back to cited text no. 15
    
16.Guijarro C, Egido J. Transcription factor- k B (NF- k B) and renal disease. Kidney Int 2001;59: 415-24.  Back to cited text no. 16
    

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Correspondence Address:
M S Roopakala
Department of Physiology, M. S. Ramaiah Medical College, MSR Nagar, Bangalore - 54, Karnataka
India
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PMID: 22382220

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    Tables

  [Table 1], [Table 2], [Table 3]

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    Abstract
   Introduction
    Materials and Me...
   Statistical Analysis
   Results
   Discussion
    References
    Article Tables
 

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