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Diagnostic Value of the Combined Measurement of Serum Hcy, Serum Cys C, and Urinary Microalbumin in Type 2 Diabetes Mellitus with Early Complicating Diabetic Nephropathy

DOI: 10.1155/2013/407452

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Abstract:

Diabetic nephropathy (DN) is a major cause of end-stage kidney disease, and therefore early diagnosis and intervention may help reverse renal damage. One hundred and sixty-eight patients with T2DM and 56 healthy volunteers (control group) were enrolled at Shandong University Qilu Hospital between April 2010 and October 2012. All subjects underwent blood sampling for sera homocysteine (Hcy) and cystatin C (Cys C) assays and a urine microalbumin test. The patients were divided into three groups according to the urine microalbumin excretion rate (UMAER): the simple DM group (SDM group, ), the early-stage DN group (EDN group, ), and the clinical DN and renal failure group (CDN group, ). Correlation analysis was performed to examine the association between sera Hcy and Cys C levels with UMAER. Our findings showed that sera Hcy level, Cys C level, and UMAER increased significantly in the SDM group ( , ), the EDN group ( ), and the CDN group ( ) as compared with the control group. These three biochemical markers also increased significantly with DN progression ( ). Correlation analysis showed that sera Hcy and Cys C levels were positively correlated with UMAER ( , ; , ). In conclusion, our results showed that sera Hcy and Cys C levels increased consistently with the development and progression of DN as indicated by UMAER. Sera Hcy and Cys C are sensitive biomarkers for the detection of early-stage DN and monitoring its progression. 1. Introduction Diabetic nephropathy (DN) is a major microvascular complication of diabetes mellitus. Renal damage may underlie early-stage DN, which, in most cases, is asymptomatic. Proteinuria is present in patients with advanced stage DN. Early detection and intervention in diabetic patients with DN will possibly reverse, or even eliminate, underlying renal damage. Therefore, the early diagnosis and treatment of DN are crucial [1, 2]. The urine microalbumin excretion rate (UMAER) is a traditional standard measure for evaluating glomerular filtration and is helpful for detecting early-stage DN and monitoring its progression. However, a combination of biomarkers is needed to improve the prediction of DN in clinical practice. Recent studies have suggested that DN is a chronic inflammatory disorder mediated by a series of cytokines, including interleukin-6, interleukin-8, and tumor necrosis factor-α as well as homocysteine (Hcy) and cystatin C (Cys C). Homocysteinemia is an independent risk factor for cardiovascular diseases [3] and has been reported in patients with chronic kidney diseases [4]. Hcy is thought to be associated with

References

[1]  A. S?mann and G. Wolf, “Diabetic nephropathy,” Internist, vol. 53, no. 10, pp. 1195–1206, 2012.
[2]  J. Menne and H. Haller, “Diabetic nephropathy,” Internist, vol. 52, no. 5, pp. 495–504, 2011.
[3]  A. Wa?kiewicz, E. Sygnowska, and G. Broda, “Homocysteine concentration and the risk of death in the adult Polish population,” Kardiologia Polska, vol. 70, no. 9, pp. 897–902, 2012.
[4]  M. Kerkeni, A. Letaief, A. Achour, A. Miled, F. Trivin, and K. Maaroufi, “Hyperhomocysteinemia, paraoxonase concentration and cardiovascular complications in Tunisian patients with nondiabetic renal disease,” Clinical Biochemistry, vol. 42, no. 9, pp. 777–782, 2009.
[5]  T. Karabag, A. Kaya, A. Temizhan, F. Ko?, S. Yavuz, and S. ?am, “The influence of homocysteine levels on endothelial function and their relation with microvascular complications in T2DM patients without macrovascular disease,” Acta Diabetologica, vol. 44, no. 2, pp. 69–75, 2007.
[6]  P. E. Lazzerini, P. L. Capecchi, E. Selvi et al., “Hyperhomocysteinemia: a cardiovascular risk factor in autoimmune diseases?” Lupus, vol. 16, no. 11, pp. 852–862, 2007.
[7]  R. Hillenbrand, A. Hillenbrand, F. Liewald, and J. Zimmermann, “Hyperhomocysteinemia and recurrent carotid stenosis,” BMC Cardiovascular Disorders, vol. 8, article 1, 2008.
[8]  P. E. Lazzerini, P. L. Capecchi, E. Selvi et al., “Hyperhomocysteinemia, inflammation and autoimmunity,” Autoimmunity Reviews, vol. 6, no. 7, pp. 503–509, 2007.
[9]  U. Alehagen, U. Dahlstr?m, and T. L. Lindahl, “Cystatin C and NT-proBNP, a powerful combination of biomarkers for predicting cardiovascular mortality in elderly patients with heart failure: results from a 10-year study in primary care,” European Journal of Heart Failure, vol. 11, no. 4, pp. 354–360, 2009.
[10]  H. Naruse, J. Ishii, T. Kawai et al., “Cystatin C in acute heart failure without advanced renal impairment,” American Journal of Medicine, vol. 122, no. 6, pp. 566–573, 2009.
[11]  C. Y. Campbell, W. Clarke, H. Park, N. Haq, B. B. Barone, and D. J. Brotman, “Usefulness of cystatin C and prognosis following admission for acute heart failure,” American Journal of Cardiology, vol. 104, no. 3, pp. 389–392, 2009.
[12]  C. Kim, “Managing women with gestational diabetes mellitus in the postnatal period,” Diabetes, Obesity and Metabolism, vol. 12, no. 1, pp. 20–25, 2010.
[13]  M. Haneda, “Diabetic nephropathy: diagnostic criteria and staging,” Nihon Rinsho Geka Gakkai Zasshi, vol. 63, supplement 6, pp. 320–323, 2005.
[14]  M. Horio, E. Imai, Y. Yasuda, T. Watanabe, and S. Matsuo, “Performance of serum cystatin C versus serum creatinine as a marker of glomerular filtration rate as measured by inulin renal clearance,” Clinical and Experimental Nephrology, vol. 15, no. 6, pp. 868–876, 2011.
[15]  O. O. I??klar, B. Barutcuo?lu, C. Kabaro?lu et al., “Do cardiac risk factors affect the homocysteine and asymmetric dimethylarginine relationship in patients with coronary artery diseases?” Clinical Biochemistry, vol. 45, no. 16-17, pp. 1325–1330, 2012.
[16]  T. Huang, S. Asimi, D. Lou, and D. Li, “Plasma phospholipid polyunsaturated fatty acids and homocysteine in Chinese type 2 diabetes patients,” Asia Pacific Journal of Clinical Nutrition, vol. 21, no. 3, pp. 394–399, 2012.
[17]  Z. Banecka-Majkutewicz, W. Sawula, L. Kadziński, A. W?grzyn, and B. Banecki, “Homocysteine, heat shock proteins, genistein and vitamins in ischemic stroke—pathogenic and therapeutic implications,” Acta Biochimica Polonica, vol. 59, no. 4, pp. 495–499, 2012.
[18]  B. Ozmen, D. Ozmen, N. Turgan, S. Habif, I. Mutaf, and O. Bayindir, “Association between homocysteinemia and renal function in patients with type 2 diabetes mellitus,” Annals of Clinical and Laboratory Science, vol. 32, no. 3, pp. 279–286, 2002.
[19]  C. Zoccali and K. J. Jager, “Hyperhomocysteinemia: a renal and cardiovascular risk factor?” Nature Reviews. Nephrology, vol. 6, no. 12, pp. 695–696, 2010.
[20]  V. A. Fonseca, L. M. Fink, and P. A. Kern, “Insulin sensitivity and plasma homocysteine concentrations in non-diabetic obese and normal weight subjects,” Atherosclerosis, vol. 167, no. 1, pp. 105–109, 2003.
[21]  D. Hucks, R. C. Thuraisingham, M. J. Raftery, and M. M. Yaqoob, “Homocysteine induced impairment of nitric oxide-dependent vasorelaxation is reversible by the superoxide dismutase mimetic TEMPOL,” Nephrology Dialysis Transplantation, vol. 19, no. 8, pp. 1999–2005, 2004.
[22]  L. Jin, R. B. Caldwell, T. Li-Masters, and R. W. Caldwell, “Homocysteine induces endothelial dysfunction via inhibition of arginine transport,” Journal of Physiology and Pharmacology, vol. 58, no. 2, pp. 191–206, 2007.
[23]  T.-H. Lan, Z.-W. Xu, Z. Wang, Y.-L. Wu, W.-K. Wu, and H.-M. Tan, “Ginsenoside Rb1 prevents homocysteine-induced endothelial dysfunction via PI3K/Akt activation and PKC inhibition,” Biochemical Pharmacology, vol. 82, no. 2, pp. 148–155, 2011.
[24]  A. Araki, “Homocysteine and diabetic macroangiopathy,” Nihon Rinsho Geka Gakkai Zasshi, vol. 64, no. 11, pp. 2153–2158, 2006.
[25]  P. Delanaye, E. Cavalier, O. Moranne, L. Lutteri, J. M. Krzesinski, and O. Bruyère, “Creatinine-or cystatin C-based equations to estimate glomerular filtration in the general population: impact on the epidemiology of chronic kidney disease,” BMC Nephrology, vol. 14, no. 1, article 57, 2013.
[26]  M. Horio, E. Imai, Y. Yasuda, T. Watanabe, and S. Matsuo, “GFR estimation using standardized serum cystatin C in Japan,” American Journal of Kidney Diseases, vol. 61, no. 2, pp. 197–203, 2013.
[27]  J. S. Kim, M. K. Kim, J. Y. Lee, B. G. Han, S. O. Choi, and J. W. Yang, “The effects of proteinuria on urinary cystatin-C and glomerular filtration rate calculated by serum cystatin-C,” Renal Failure, vol. 34, no. 6, pp. 676–684, 2012.
[28]  P. K. Dabla, “Renal function in diabetic nephropathy,” World Journal of Diabetes, vol. 1, no. 2, pp. 48–56, 2010.

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