Journal of Diabetes & Metabolic Disorders | |
The relationship between glycemic control, beta2-microglobulin and inflammation in patients on maintenance dialysis treatment | |
Despina Kyriaki2  Vaia D Raikou1  | |
[1] 1st Department of Medicine - Propaedaetic, National and Kapodistrian University of Athens, School of Medicine, 17 Agiou Thoma, Αthens, Greece;Department of Nuclear Medicine, General Hospital “LAΪKO”, Αthens, Greece | |
关键词: Dialysis; Inflammation; Beta2-microglobulin; Glycemic control; | |
Others : 1212330 DOI : 10.1186/s40200-015-0162-1 |
|
received in 2014-02-06, accepted in 2015-04-14, 发布年份 2015 | |
【 摘 要 】
Background
Hyperglycemia appears to play a significant role on the inflammatory cytokines production. Beta2-microglobulin (beta2M) is accumulated in the circulation of dialysis patients. We studied the relationship between glycemic control defined by glucose serum concentrations and insulin resistance, beta2M and markers of inflammation in patients on renal replacement therapies with or/and without diabetes mellitus.
Methods
We enrolled 96 dialyzed patients, 62 males and 34 females. The treatment modalities which were applied were : regular hemodialysis (HD, n = 34), predilution hemodiafiltration (HDF, n = 42) and peritoneal dialysis (PD, n = 20). Dialysis adequacy was defined by Kt/V for urea.Beta2M and insulin serum concentrations were measured by radioimmunoassays. hsCRP and TNF-α serum concentrations were measured by ELISA. Insulin resistance was calculated using the homeostasis model assessment of insulin resistance (HOMA-IR).We examined the association of elevated serum glucose with inflammatory factors and we built a multivariable model to investigate if glucose could be a potential determinant of beta2M serum levels.
Results
Serum glucose was positively correlated with beta2M and TNF-α (r = 0.320, p = 0.002 and r = 0.215, p = 0.03 respectively).We observed significant association between the patients with higher serum glucose concentrations and the patients with greater beta2Μ concentrations (x2 = 4.44, p = 0.03). Multivariable model showed that glucose acts as a significant independent determinant of beta2M adjusting for age, gender, dialysis modality and metabolic acidosis status.
Conclusions
The elevated glucose concentrations were positively associated with both, greater beta2M serum concentrations and up-regulated inflammatory procedure in dialysis patients with or/and without diabetes mellitus.
【 授权许可】
2015 Raikou and Kyriaki; licensee BioMed Central.
【 预 览 】
Files | Size | Format | View |
---|---|---|---|
20150614090838355.pdf | 554KB | download | |
Figure 2. | 13KB | Image | download |
Figure 1. | 23KB | Image | download |
【 图 表 】
Figure 1.
Figure 2.
【 参考文献 】
- [1]Kazama JJ, Maruyama H, Gejyo F. Reduction of circulating beta2-microglobulin level for the treatment of dialysis-related amyloidosis. Nephrol Dial Transplant. 2001; 16(suppl 4):31-5.
- [2]Fang ZY, Prins JB, Marwick TH. Diabetic cardiomyopathy: evidence, mechanisms, and therapeutic implications. Endocr Rev. 2004; 25:543-67.
- [3]Gaede P, Vedel P, Larsen N, Jensen GV, Parving HH, Pedersen O. Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes. N Engl J Med. 2003; 348:383-93.
- [4]Ritz E, Wanner C. The challenge of sudden death in dialysis patients. Clin J Am Soc Nephrol. 2008; 3:920-9.
- [5]Ansari A, Thomas S, Goldsmith D. Assessing glycemic control in patients with diabetes and end-stage renal failure. Am J Kidney Dis. 2003; 41:523-31.
- [6]Kovesdy CP, Park JC, Kalantar-Zadeh K. Glycemic control and burnt-out diabetes in ESRD. Semin Dial. 2010; 23:148-56.
- [7]Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med. 2008; 358:2560-72.
- [8]KDOQI clinical practice guidelines and clinical practice recommendations for diabetes and chronic kidney disease. Am J Kidney Dis. 2007; 49:S12-154.
- [9]Ismail-Beigi F, Craven T, Banerji MA, Basile J, Calles J, Cohen RM et al.. Effect of intensive treatment of hyperglycaemia on microvascular outcomes in type 2 diabetes: an analysis of the ACCORD randomised trial. Lancet. 2010; 376:419-30.
- [10]Chauveau P, Nguyen H, Combe C, Chêne G, Azar R, Cano N et al.. French Study Group for Nutrition in Dialysis.Dialyzer membrane permeability and survival in hemodialysis patients. Am J Kidney Dis. 2005; 45:565-71.
- [11]Daugirdas JT. Second generation logarithmic estimates of single-pool variable volume Kt/V: an analysis of error. J Am Soc Nephrol. 1993; 4:1205-13.
- [12]Silva EA, Flexa F, Zanella MT. Impact of abdominal fat and insulin resistance on arterial hypertension in non-obese women. MT Arq Bras Endocrinol Metabol. 2009; 53(3):340-3.
- [13]Daugirdas JT. Simplified equations for monitoring Kt/V, PCRn, eKt/V, and ePCRn. Adv Ren Replace Ther. 1995; 2:295-304.
- [14]Kirschbaum B. Spurious metabolic acidosis in hemodialysis patients. Am J Kidney Dis. 2000; 35:1068-71.
- [15]Johansen JS, Harris AK, Rychly DJ, Ergul A. Oxidative stress and the use of antioxidants in diabetes: linking basic science to clinical practice. Cardiovasc Diabetol. 2005; 4:5. BioMed Central Full Text
- [16]Tzoulaki I, Murray GD, Lee AJ, Rumley A, Lowe GD, Fowkes FG. C-reactive protein, interleukin-6, and soluble adhesion molecules as predictors of progressive peripheral atherosclerosis in the general population: Edinburgh Artery Study. Circulation. 2005; 112:976-83.
- [17]Wilson AM, Kimura E, Harada RK, Nair N, Narasimhan B, Meng XY et al.. Beta2-microglobulin as a biomarker in peripheral arterial disease: proteomic profiling and clinical studies. Circulation. 2007; 116:1396-403.
- [18]Miyata T, Inagi R, Iida Y, Sato M, Yamada N. Oda 0, Maeda K, Seo H: Involvement of β2-microgbobulin modified with advanced glycation end products in the pathogenesis of hemodialysis- associated amyboidosis. J Clin Invest. 1994; 93:521-8.
- [19]Kalantar-Zadeh K, Mehrotra R, Fouque D, Kopple JD. Metabolic acidosis and malnutrition- inflammation complex syndrome in chronic renal failure. Semin Dial. 2004; 17:455-65.
- [20]Sonikian M, Gogusev J, Zingraff J, Loric S, Quednau B, Bessou G et al.. Potential effect of metabolic acidosis on beta2- microglobulin generation: in vivo and in vitro studies. J Am Soc Nephrol. 1996; 7:350-6.
- [21]Stanga Z, Nock S, Medina-Escobar P, Nydegger UE, Risch M, Risch L. Factors other than the glomerular filtration rate that determine the serum beta-2-microglobulin level. PLoS One. 2013; 8(8):e72073.
- [22]London GM, Drueke TB. Atherosclerosis and arteriosclerosis in chronic renal failure. Kidney Int. 1997; 51(6):1678-95.
- [23]Mehrotra R, Kopple J. Causes of protein-energy malnutrition in chronic renal failure. In: Nutritional Management of Renal Disease, ed 2. Kopple J, Massry S, editors. Lippincott, Williams & Wilkins, Philadelphia; 2003: p.167-82.
- [24]Vanholder R, Laecke SV, Verbeke F, Glorieux G, Biesen WV. Uraemic toxins and cardiovascular disease: in vitro research versus clinical studies. Nephrol Dial Transplant Plus. 2008; 1:2-10.
- [25]Okuno S, Ishimura E, Kohno K, Fujino-Katoh Y, Maeno Y, Yamakawa T et al.. Serum beta2-microglobulin level is a significant predictor of mortality in maintenance haemodialysis patients. Nephrol Dial Transplant. 2009; 24(2):571-7.