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400042 重庆, 第三军医大学大坪医院野战外科研究所肾内科
[何娅妮, E-mail: heynmail@163.com HE Yani, E-mail: heynmail@163.com
收稿:2017-06-22,
修回:2017-07-13,
纸质出版:2017-10-30
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胡威, 陈佳, 林利容, 等. 尿DcR2/Cr评价IgA肾病肾小管间质损伤程度[J]. 第三军医大学学报, 2017,39(20):2030-2034.
Wei HU, Jia CHEN, Lirong LIN, et al. Urinary DcR2/Cr in evaluation of renal tubulointerstitial injury for IgA nephropathy[J]. Journal of Third Military Medical University, 2017, 39(20): 2030-2034.
胡威, 陈佳, 林利容, 等. 尿DcR2/Cr评价IgA肾病肾小管间质损伤程度[J]. 第三军医大学学报, 2017,39(20):2030-2034. DOI: 10.16016/j.1000-5404.201706113.
Wei HU, Jia CHEN, Lirong LIN, et al. Urinary DcR2/Cr in evaluation of renal tubulointerstitial injury for IgA nephropathy[J]. Journal of Third Military Medical University, 2017, 39(20): 2030-2034. DOI: 10.16016/j.1000-5404.201706113.
目的
2
探讨尿DcR2/Cr是否可作为反映IgA肾病(IgA nephropathy,IgAN)肾间质损伤的生物标志物。
方法
2
纳入2016年我院经肾活检诊断为原发性IgAN的患者210例,选取同期我院体检中心健康体检者80例作为对照组。收集2组人口学资料、临床数据。按照牛津分型评估IgAN患者肾组织损伤程度。采用酶联免疫吸附测定方法检测血清及尿液中DcR2水平,将尿DcR2/Cr值三分位后分析不同慢性肾脏病(chronic kidney disease
CKD)分期的患者及间质损伤程度的百分比,ROC曲线分析尿DcR2/Cr评估IgAN肾小管间质损伤的敏感性及特异性。
结果
2
IgAN中尿DcR2/Cr水平较对照组增加,而血清DcR2水平与对照组比较差异无统计学意义。据IgAN组尿DcR2/Cr值三分位后分析发现,尿DcR2/Cr < 130 ng/g时CKD1~2期和T0期百分率最高,尿DcR2/Cr>201 ng/g时CKD4~5期和T2期百分率最高。相关性分析表明尿DcR2/Cr与尿微量白蛋白/肌酐(ACR)、uNAG/Cr、肾小管间质损伤呈正相关,与肾小球率过滤(e-GFR)呈负相关。ROC曲线分析表明尿DcR2/Cr用于评估肾小管间质损伤的曲线下面积为0.907,敏感性为87.0%,特异性为80.5%。
结论
2
尿DcR2/Cr水平在IgA肾病T2期较T0期的明显增加,其与IgAN肾功能及肾小管间质损伤程度密切相关,是评价IgAN肾小管间质损伤潜在的生物标志物。
Objective
2
To investigate whether urinary decoy receptor 2 (uDcR2) could be used as a biomarker for assessing renal tubulointerstitial injury in IgA nephropathy (IgAN) patients.
Methods
2
A total of 210 patients who were diagnosed as primary IgAN by renal biopsy in our hospital in 2016 were recruited. Meanwhile 80 healthy participates were assigned into control group. The severity of IgA nephropathy was evaluated by using the Oxford-MEST classification system. The serum and urinary DcR2 levels were measured by enzyme-linked immunosorbent assay (ELISA). The IgAN patients were stratified into 3 subgroups according to the uDcR2/creatinine(Cr) level. Percentages of patients with different stages of chronic kidney disease (CKD) and severity of tubulointerstitial injury were compared. The sensitivity and specificity of uDcR2 for evaluating tubulointerstitial injury was analyzed by receiver operating characteristic (ROC) curve.
Results
2
Compare with the control
uDcR2 level in the IgAN group was higher
but there was no significant difference in serum DcR2 between the 2 groups. Among the IgAN subgroups
the percentages of patients with CKD 1~2 and T0 were the highest when uDcR2/Cr was < 130 ng/g. When uDcR2/Cr was >201 ng/g
the majority of patients were in stage of CKD 4~5 and T2. The correlation analysis showed that uDcR2 level was positively associated with albumin/creatinine ratio (ACR)
urinary N-acetyl-beta-D-glucosaminidase (uNAG)/Cr and scores of renal tubulointerstitial injury. It was negatively correlated to estimated glomerular filtration rates (eGFR). The area of under the curve (AUC) of uDcR2/Cr was 0.907
which was higher than the AUCs of eGFR
uNAG/Cr and ACR. The sensitivity and specificity of uDcR2/Cr were 87.0% and 80.5%
respectively.
Conclusion
2
The uDcR2 level in T2 of IgA nephropathy is obviously higher than that in T0
which is closely associated with the severity of renal tubulointerstitial injury and renal function parameters. This suggests that uDcR2 could serve as a potential biomarker to evaluate the tubulointerstitial injury in IgAN patients.
SHU D, XU F, SU Z, et al. Risk factors of progressive IgA nephropathy which progress to end stage renal disease within ten years: a case-control study[J]. BMC Nephrol, 2017, 18(1): 11. DOI: 10.1186/s12882-016-0429-x.
RODRIGUES J C, HAAS M, REICH H N. IgA Nephropathy[J]. Clin J Am Soc Nephrol, 2017, 12(4): 677-686. DOI: 10.2215/CJN.07420716.
FABIANO R C, ARAUJO S A, BAMBIRRA E A, et al. The Oxford Classification predictors of chronic kidney disease in pediatric patients with IgA nephropathy[J]. J Pediatr (Rio J), 2017. DOI: 10.1016/j.jped.2016.09.003.
MAIXNEROVA D, REILY C, BIAN Q, et al. Markers for the progression of IgA nephropathy[J]. J Nephrol, 2016, 29(4): 535-541. DOI: 10.1007/s40620-016-0299-0.
FLYVBJERG A. Diabetic angiopathy, the complement system and the tumor necrosis factor superfamily[J]. Nat Rev Endocrinol, 2010, 6(2): 94-101. DOI: 10.1038/nrendo.2009.266.
YANG Z C, MA J. Actein enhances TRAIL effects on suppressing gastric cancer progression by activating p53/Caspase-3 signaling[J]. Biochem Biophys Res Commun, 2016. DOI: 10.1016/j.bbrc.2016.11.162.
SANCHEZ-LAZARO I J, ALMENAR-BONET L, ROMERO-PELECHANO A, et al. Serum markers of apoptosis in the early period of heart transplantation[J]. Biomarkers, 2012, 17(3): 254-260. DOI: 10.3109/1354750X.2012.664168.
YUZAWA Y, YAMAMOTO R, TAKAHASHI K, et al. Evidence-based clinical practice guidelines for IgA nephropathy 2014[J]. Clin Exp Nephrol, 2016, 20(4): 511-535. DOI: 10.1007/s10157-015-1223-y.
METHVEN S, GASPARINI A, CARRERO J J, et al. Routinely measured iohexol glomerular filtration rate versus creatinine-based estimated glomerular filtration rate as predictors of mortality in patients with advanced chronic kidney disease: a Swedish Chronic Kidney Disease Registry cohort study[J]. Nephrol Dial Transplant, 2017. DOI: 10.1093/ndt/gfw457.
HWANG J H, LEE J P, KIM C T, et al. Urinary Periostin Excretion Predicts Renal Outcome in IgA Nephropathy[J]. Am J Nephrol, 2016, 44(6): 481-492. DOI: 10.1159/000452228.
TRIMARCHI H, BARRATT J, CATTRAN D C, et al. Oxford Classification of IgA nephropathy 2016-the role of crescentic lesions: an update from the IgA Nephropathy Classification Working Group[J]. Kidney Int, 2017. DOI: 10.1016/j.kint.2017.02.003.
KATAFUCHI R, NINOMIYA T, NAGATA M, et al. Validation study of oxford classification of IgA nephropathy: the significance of extracapillary proliferation[J]. Clin J Am Soc Nephrol, 2011, 6(12): 2806-2813. DOI: 10.2215/CJN.02890311.
[WOO K T, LIM C C, FOO M W, et al. 30-year follow-up study of IgA nephritis in a Southeast Asian population: an evaluation of the Oxford histological classification[J ] . Clin Nephrol, 2016, 86 (2016)(11): 270-278. DOI: 10.5414/cn108891. http://dx.doi.org/10.5414/cn108891.
COPPO R. Biomarkers and targeted new therapies for IgA nephropathy[J]. Pediatr Nephrol, 2017, 32(5): 725-731. DOI: 10.1007/s00467-016-3390-9.
FERENBACH D A, BONVENTRE J V. Acute kidney injury and chronic kidney disease: From the laboratory to the clinic[J]. Nephrol Ther, 2016, 12 Suppl 1: S41-48. DOI: 10.1016/j.nephro.2016.02.005.
LIU J, YANG J R, HE Y N, et al. Accelerated senescence of renal tubular epithelial cells is associated with disease progression of patients with immunoglobulin A (IgA) nephropathy[J]. Transl Res, 2012, 159(6): 454-463. DOI: 10.1016/j.trsl.2011.11.008.
SAGIV A, BIRAN A, YON M, et al. Granule exocytosis mediates immune surveillance of senescent cells[J]. Oncogene, 2013, 32(15): 1971-1977. DOI: 10.1038/onc.2012.206.
E O R, TIRINCSI A, LOGUE S E, et al. The Janus Face of Death Receptor Signaling during Tumor Immunoediting[J]. Front Immunol, 2016, 7: 446. DOI: 10.3389/fimmu.2016.00446.
CHEN J, ZHANG W W, CHEN K H, et al. Urinary DcR2 is a novel biomarker for tubulointerstitial injury in patients with diabetic nephropathy[J]. Am J Physiol Renal Physiol, 2017, 313(2): F273-F281. DOI: 10.1152/ajprenal.00689.2016.
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