原发性膜性肾病合并肾小管间质损伤的特征分析
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摘要
目的分析原发性膜性肾病(IMN)合并肾小管间质损伤的临床特点及病理指标的关系,为临床上早期发现IMN肾小管损伤及改善其预后提供依据。方法回顾性收集2013年1月至2017年12月于首都医科大学附属北京友谊医院诊断为IMN的初治住院患者共40例,根据肾小管间质损伤程度,将患者分为轻度肾小管间质损伤组(40例)及重度肾小管间质损伤组(16例),收集患者血压、年龄、性别、血肌酐以及肾小管间质损害积分等临床资料并通过比较明确肾小管间质损伤的预测因子。结果单因素Logistic回归分析显示,合并高血压使IMN肾小管损伤的风险增加6. 33倍。血清肌酐每升高10μmmol/L、血清尿素氮每升高1 mmmol/L,预示发生肾小管损伤风险分别增加4. 83倍和1. 74倍。尿α1微球蛋白每升高1 mg/dl,预示肾小管损伤风险增加1. 33倍。将上述变量选入Logistic多因素回归模型,结果显示,仅有血清肌酐是发生严重肾小管损伤的独立预测因素,调整后的OR值为7. 20,95%CI:1. 70～30. 38,P=0. 007。结论血肌酐水平是临床表现为肾病综合征的IMN患者肾小管损伤的独立预测因子。
Objective To analyze the clinical characteristics and pathological parameters of primary membranous nephropathy( IMN with tubulointerstitial impairment,and to provide the basis for early detection of IMN renal tubular impairment in order to improve its prognosis.Methods Patients with IMN diagnosed as nephrotic syndrome were screened and divided into mild tubulointerstitial impairment group and severe tubulointerstitial impairment group. Blood pressure,age,gender,serum creatinine and tubulointerstitial damage scores were collected. These indicators were compared for the prediction of renal tubular interstitial impairment. Results Univariate Logistic regression analysis showed that hypertension combined increased the risk of IMN tubular impairment by 6. 33 times. For every increase10 μmmol/L of serum creatinine and increase 1 mmmol/L in serum urea nitrogen,the risk of renal tubular impairment increased by 4. 83 times and 1. 74 times,respectively. Each 1 mg/dl increase in urinary α1 microglobulin predicted 1. 33 times increase in the risk of tubular impairment The above variables were selected into the logistic multivariate regression model. The results suggest that only serum creatinine is an independent predictor of severe tubular damage. The adjusted OR is 7. 20,95% CI: 1. 70 ～ 30. 38,P = 0. 007. Conclusion Serum level of creatinine is independent predictor for renal tubular impairment in IMN patients with clinical manifestations of nephrotic syndrome.
Objective To analyze the clinical characteristics and pathological parameters of primary membranous nephropathy( IMN with tubulointerstitial impairment,and to provide the basis for early detection of IMN renal tubular impairment in order to improve its prognosis.Methods Patients with IMN diagnosed as nephrotic syndrome were screened and divided into mild tubulointerstitial impairment group and severe tubulointerstitial impairment group. Blood pressure,age,gender,serum creatinine and tubulointerstitial damage scores were collected. These indicators were compared for the prediction of renal tubular interstitial impairment. Results Univariate Logistic regression analysis showed that hypertension combined increased the risk of IMN tubular impairment by 6. 33 times. For every increase10 μmmol/L of serum creatinine and increase 1 mmmol/L in serum urea nitrogen,the risk of renal tubular impairment increased by 4. 83 times and 1. 74 times,respectively. Each 1 mg/dl increase in urinary α1 microglobulin predicted 1. 33 times increase in the risk of tubular impairment The above variables were selected into the logistic multivariate regression model. The results suggest that only serum creatinine is an independent predictor of severe tubular damage. The adjusted OR is 7. 20,95% CI: 1. 70 ～ 30. 38,P = 0. 007. Conclusion Serum level of creatinine is independent predictor for renal tubular impairment in IMN patients with clinical manifestations of nephrotic syndrome.
引文
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[13] Bienia!s B,Zajczkowska M,Borzcka H,et al. Early Markers of Tubulointerstitial Fibrosis in Children With Idiopathic Nephrotic Syndrome:Preliminary Report[J]. Medicine(Baltimore),2015,94(42):e1746.
[14] Sharma M,Gupta S,Singh K,et al. Association of glutathione-Stransferase with patients of type 2 diabetes mellitus with and without nephropathy[J]. Diabetes Metab Syndr,2016,10(4):194-197.
[15] Zhang Y,Li A,Wen J,et al. Kidney Injury Molecule-1 Level is Associated with the Severity of Renal Interstitial Injury and Prognosis in Adult Henoch-Schnlein Purpura Nephritis[J]. Arch Med Res,2017,48(5):449-458.
[16] Nakagawa S. Identification of Biomarkers for Tubular Injury and Interstitial Fibrosis in Chronic Kidney Disease[J]. Yakugaku Zasshi,2017,137(11):1355-1360.
[17] Maas RJ,van den Brand JA,Waanders F,et al. Kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin as prognostic markers in idiopathic membranous nephropathy[J]. Ann Clin Biochem,2016,53(Pt 1):51-57.
[18] Zhang H,Wang F,Xiao H,et al. The ratio of urinaryα1-microglobulin to microalbumin can be used as a diagnostic criterion for tubuloproteinuria[J]. Intractable Rare Dis Res,2018,7(1):46-50.
[2]郭燕,刁宗礼,刘文虎.北京地区单中心2009~2016年肾脏病理疾病谱特征分析[J].中国临床医生杂志,2017,45(6):58-61.
[3] Horvatic I,Ljubanovic DG,Bulimbasic S,et al. Prognostic significance of glomerular and tubulointerstitial morphometry in idiopathic membranous nephropathy[J]. Pathol Res Pract,2012,208(11):662-667.
[4] Bazzi C,Petrini C,Rizza V,et al. A modern approach to selectivity of proteinuria and tubulointerstitial damage in nephrotic syndrome[J].Kidney Int,2000,58(4):1732-1741.
[5] Li Y,Wang J,Zhu X,et al. Urinary protein markers predict the severity of renal histological lesions in children with mesangial proliferative glomerulonephritis[J]. BMC Nephrol,2012,13:29.
[6]刘伏友,李瑛,杨丽,等.成人原发性肾病综合征肾小管间质损害的危险因素分析[J].中华肾脏病杂志,2006,22(5):293-294.
[7] Yang Y,Zhang Z,Zhuo L,et al. The Spectrum of Biopsy-Proven Glomerular Disease in China:A Systematic Review[J]. Chin Med J(Engl),2018,131(6):731-735.
[8] Pan X,Xu J,Ren H,et al. Changing spectrum of biopsy-proven primary glomerular diseases over the past 15 years:a single-center study in China[J]. Contrib Nephrol,2013,181:22-30.
[9] Hou JH,Zhu HX,Zhou ML,et al. Changes in the Spectrum of Kidney Diseases:An Analysis of 40,759 Biopsy-Proven Cases from 2003 to2014 in China[J]. Kidney Dis(Basel),2018,4(1):10-19.
[10] Zhang BO,Cheng M,Yang M,et al. Analysis of the prognostic risk factors of idiopathic membranous nephropathy using a new surrogate end-point[J]. Biomed Rep,2016,4(2):147-152.
[11] Chen Y,Tang L,Feng Z,et al. Pathological predictors of renal outcomes in nephrotic idiopathic membranous nephropathy with decreased renal function[J]. J Nephrol,2014,27(3):307-316.
[12] Shin YJ,Kim KA,Kim ES,et al. Identification of aldo-keto reductase(AKR7A1)and glutathione S-transferase pi(GSTP1)as novel renal damage biomarkers following exposure to mercury[J]. Hum Exp Toxicol,2017,37(10):1025-1036.
[13] Bienia!s B,Zajczkowska M,Borzcka H,et al. Early Markers of Tubulointerstitial Fibrosis in Children With Idiopathic Nephrotic Syndrome:Preliminary Report[J]. Medicine(Baltimore),2015,94(42):e1746.
[14] Sharma M,Gupta S,Singh K,et al. Association of glutathione-Stransferase with patients of type 2 diabetes mellitus with and without nephropathy[J]. Diabetes Metab Syndr,2016,10(4):194-197.
[15] Zhang Y,Li A,Wen J,et al. Kidney Injury Molecule-1 Level is Associated with the Severity of Renal Interstitial Injury and Prognosis in Adult Henoch-Schnlein Purpura Nephritis[J]. Arch Med Res,2017,48(5):449-458.
[16] Nakagawa S. Identification of Biomarkers for Tubular Injury and Interstitial Fibrosis in Chronic Kidney Disease[J]. Yakugaku Zasshi,2017,137(11):1355-1360.
[17] Maas RJ,van den Brand JA,Waanders F,et al. Kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin as prognostic markers in idiopathic membranous nephropathy[J]. Ann Clin Biochem,2016,53(Pt 1):51-57.
[18] Zhang H,Wang F,Xiao H,et al. The ratio of urinaryα1-microglobulin to microalbumin can be used as a diagnostic criterion for tubuloproteinuria[J]. Intractable Rare Dis Res,2018,7(1):46-50.