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IgA肾病是世界上最常见的一种原发性肾小球肾炎。尽管大多数病人预后良好,仍有15%~25%的IgA肾病在诊断10年之内进展至终末期肾衰竭[1-3]。新近研究[4-5]发现,吸烟不仅是动脉粥样硬化疾病的高危因素,也是慢性肾脏病(CKD)进展中的独立危险因素,是影响CKD预后的主要因素之一,并存在剂量-效应关系[4-5]。本文主要研究吸烟对IgA肾病的临床及肾脏病理指标的影响,探讨吸烟在IgA肾病慢性进展的作用。
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2组病人收缩压、舒张压、平均动脉压、血IgA、血白蛋白、总胆固醇、尿转铁蛋白、尿N-乙酰-β-D葡萄糖苷酶、尿白蛋白排泄率、尿免疫球蛋白IgG差异无统计学意义(P>0.05),吸烟组eGFR明显低于非吸烟组(P < 0.01),年龄、男性比例、三酰甘油、血糖和尿β2微球蛋白、α1微球蛋白、24 h尿蛋白均高于非吸烟组(P < 0.05~P < 0.01)(见表 1)。
指标 非吸烟组(n=119) 吸烟组(n=30) t P 年龄/岁 35.47±11.44 42.33±8.90 4.23 < 0.01 性别(男) 30(25.21) 29(96.67) 51.15* < 0.01 收缩压/mmHg 130.90±14.71 127.73±15.87 1.31 >0.05 舒张压/mmHg 87.65±12.53 87.43±11.04 0.12 >0.05 平均动脉压/mmHg 102.06±12.46 100.86±12.07 0.62 >0.05 血IgA/(g/L) 2.61±1.05 2.42±0.74 1.33 >0.05 24 h尿蛋白/(g/24 h) 2.01±2.41 2.92±3.32 1.98 < 0.05 血白蛋白(g/L) 38.53±7.17 36.75±9.19 1.36 >0.05 总胆固醇/(mmol/L) 5.11±1.64 5.64±2.43 1.62 >0.05 三酰甘油/(mmol/L) 1.74±1.00 2.51±1.16 4.54 < 0.01 eGFR/[mL/(min·1.73 m2)] 82.06±32.33 69.00±26.27 2.80 < 0.01 血糖/(mmol/L) 4.88±0.63 5.26±1.35 2.32 < 0.05 尿β2微球蛋白/(mg/L) 0.41±0.47 0.71±0.72 3.17 < 0.01 尿α1微球蛋白/(mg/L) 15.05±16.19 25.86±27.98 2.99 < 0.01 尿转铁蛋白/(mg/L) 38.67±26.95 32.51±21.07 1.61 >0.05 尿N-乙酰-β-D葡萄糖苷酶/(U/L) 21.98±20.09 25.86±21.19 1.19 >0.05 尿白蛋白排泄率/(mg/L) 963.66±807.30 1 102.37±886.80 1.03 >0.05 尿免疫球蛋白IgG/(mg/L) 123.99±137.30 154.11±209.30 1.08 >0.05 *示χ2值 表 1 各项临床指标在2组病人中比较(x±s)
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2组病人肾小球局灶性硬化、系膜细胞增生、系膜基质增生、细胞新月体形成、纤维新月体形成、间质炎症细胞浸润和肾小管萎缩积分差异均无统计学意义(P>0.05),吸烟组病人的肾间质纤维化积分和肾小球毛细血管壁增厚积分均高于非吸烟组(P < 0.05)(见表 2)。
指标 非吸烟组(n=119) 吸烟组(n=30) Z P 肾小球局灶性硬化/分 0 47 10 0.18 >0.05 1 37 12 9 19 5 3 16 3 系膜细胞增生/分 1 89 18 0.42 >0.05 2 37 4 3 23 8 系膜基质增生/分 1 73 17 0.69 >0.05 2 48 8 3 28 5 细胞新月体形成/分 0 86 14 1.28 >0.05 1 37 8 2 21 6 3 5 2 纤维新月体形成/分 0 89 16 0.86 >0.05 1 42 8 2 15 5 3 3 1 间质炎症细胞浸润/分 0 9 5 0.63 >0.05 1 72 15 2 28 9 3 10 1 间质纤维化/分 0 7 3 2.40 < 0.05 1 75 10 2 26 14 3 11 4 肾小管萎缩/分 0 4 2 1.15 >0.05 1 74 14 3 10 4 2 31 11 肾小球毛细血管壁增厚/分 0 35 1 6.31 < 0.05 1 114 29 表 2 肾脏病理损伤各项指标在2组病人中比较(n)
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计算30例吸烟的IgA肾病病人的累计吸烟量,将119例非吸烟IgA肾病病人的累计吸烟量计为0。Pearson相关分析结果显示,病人吸烟量与eGFR呈负相关关系(r=-0.219,P < 0.05),与肾间质纤维化积分和肾小管萎缩积分均呈正相关关系(r=0.183、0.187,P < 0.05)。
吸烟对IgA肾病临床指标及肾脏病理的影响
Effect of smoking on the clinical indicators and renal pathology of IgA nephropathy
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摘要:
目的探讨吸烟对IgA肾病临床指标和肾脏病理的影响。 方法回顾性分析149例IgA肾病病人的吸烟状态,并分析其与病人临床指标及肾脏病理损伤指标的关系。 结果149例IgA肾病病人中吸烟者30例(吸烟组),非吸烟者119例(非吸烟组)。吸烟组病人肾小球滤过率(eGFR)明显低于非吸烟组(P < 0.01),年龄、男性比例、三酰甘油、血糖和尿β2微球蛋白、α1微球蛋白、24 h尿蛋白均高于非吸烟组(P < 0.05~P < 0.01)。吸烟组病人的肾间质纤维化积分和肾小球毛细血管壁增厚积分均高于非吸烟组(P < 0.05)。Pearson相关分析显示,吸烟量与eGFR呈负相关关系(r=-0.219,P < 0.05),与肾间质纤维化积分和肾小管萎缩积分均呈正相关关系(r=0.183、0.187,P < 0.05)。 结论吸烟与IgA肾病病人肾功能损伤存在相关关系,吸烟损伤肾脏病理以肾小管间质慢性化病变为主。 Abstract:ObjectiveTo investigate the effects of smoking on the clinical indicators and renal pathology of IgA nephropathy. MethodsThe smoking status of 149 patients with IgA nephropathy was retrospectively analyzed, and its relationship with clinical indicators and renal pathological injury were analyzed. ResultsAmong 149 IgA nephropathy patients, 30 cases were smokers(smoking group)and 119 cases were non-smokers(non-smoking group).The glomerular filtration rate in smoking group was significantly lower than that in non-smoking group(P < 0.01), and the age, male ratio, and levels of triglyceride, blood glucose and urine β2 microglobulin, α1 microglobulin and 24 h urinary protein in smoking group were higher than those in non-smoking group(P < 0.05 to P < 0.01).The scores of renal interstitial fibrosis and glomerular capillary wall thickening in smoking group were higher than those in non-smoking group(P < 0.05).The results of Pearson correlation analysis showed that the smoking amount was negatively correlated with eGFR(r=-0.219, P < 0.05), and positively correlated with the scores of renal interstitial fibrosis and renal tubular atrophy(r=0.183, 0.187, P < 0.05). ConclusionsThere is a correlation between smoking and renal function injury in IgA nephropathy patients.The chronic tubular interstitial lesion is the main feature of renal pathology caused by smoking. -
Key words:
- IgA nephropathy /
- smoking /
- glomerular filtration rate /
- renal pathology
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表 1 各项临床指标在2组病人中比较(x±s)
指标 非吸烟组(n=119) 吸烟组(n=30) t P 年龄/岁 35.47±11.44 42.33±8.90 4.23 < 0.01 性别(男) 30(25.21) 29(96.67) 51.15* < 0.01 收缩压/mmHg 130.90±14.71 127.73±15.87 1.31 >0.05 舒张压/mmHg 87.65±12.53 87.43±11.04 0.12 >0.05 平均动脉压/mmHg 102.06±12.46 100.86±12.07 0.62 >0.05 血IgA/(g/L) 2.61±1.05 2.42±0.74 1.33 >0.05 24 h尿蛋白/(g/24 h) 2.01±2.41 2.92±3.32 1.98 < 0.05 血白蛋白(g/L) 38.53±7.17 36.75±9.19 1.36 >0.05 总胆固醇/(mmol/L) 5.11±1.64 5.64±2.43 1.62 >0.05 三酰甘油/(mmol/L) 1.74±1.00 2.51±1.16 4.54 < 0.01 eGFR/[mL/(min·1.73 m2)] 82.06±32.33 69.00±26.27 2.80 < 0.01 血糖/(mmol/L) 4.88±0.63 5.26±1.35 2.32 < 0.05 尿β2微球蛋白/(mg/L) 0.41±0.47 0.71±0.72 3.17 < 0.01 尿α1微球蛋白/(mg/L) 15.05±16.19 25.86±27.98 2.99 < 0.01 尿转铁蛋白/(mg/L) 38.67±26.95 32.51±21.07 1.61 >0.05 尿N-乙酰-β-D葡萄糖苷酶/(U/L) 21.98±20.09 25.86±21.19 1.19 >0.05 尿白蛋白排泄率/(mg/L) 963.66±807.30 1 102.37±886.80 1.03 >0.05 尿免疫球蛋白IgG/(mg/L) 123.99±137.30 154.11±209.30 1.08 >0.05 *示χ2值 表 2 肾脏病理损伤各项指标在2组病人中比较(n)
指标 非吸烟组(n=119) 吸烟组(n=30) Z P 肾小球局灶性硬化/分 0 47 10 0.18 >0.05 1 37 12 9 19 5 3 16 3 系膜细胞增生/分 1 89 18 0.42 >0.05 2 37 4 3 23 8 系膜基质增生/分 1 73 17 0.69 >0.05 2 48 8 3 28 5 细胞新月体形成/分 0 86 14 1.28 >0.05 1 37 8 2 21 6 3 5 2 纤维新月体形成/分 0 89 16 0.86 >0.05 1 42 8 2 15 5 3 3 1 间质炎症细胞浸润/分 0 9 5 0.63 >0.05 1 72 15 2 28 9 3 10 1 间质纤维化/分 0 7 3 2.40 < 0.05 1 75 10 2 26 14 3 11 4 肾小管萎缩/分 0 4 2 1.15 >0.05 1 74 14 3 10 4 2 31 11 肾小球毛细血管壁增厚/分 0 35 1 6.31 < 0.05 1 114 29 -
[1] USUI J, YAMAGATA K, KAI H, et al. Heterogeneity of prognosis in adult IgA nephropathy, especially with mild proteinuria or mild histological features[J]. Int Med, 2001, 40(8): 697. doi: 10.2169/internalmedicine.40.697 [2] LI PK, HO KK, SZETO CC, et al. Prognostic indicators of IgA nephropathy in the Chinese-clinical and pathological perspectives[J]. Nephrol Dial Transplant, 2002, 17(1): 64. doi: 10.1093/ndt/17.1.64 [3] MANNO C, STRIPPOLI GF, D'ALTRI C, et al. Anovel simpler histological classification for renal survival in IgA nephropathy: a retrospective study[J]. Am J Kidney Dis, 2007, 49(6): 763. doi: 10.1053/j.ajkd.2007.03.013 [4] HALLAN S, DE MUTSERT R, CARLSEN S, et al. Obesity, smoking, and physical inactivity as risk factors for CKD: are men more vulnerable?[J]. Am J Kidney Dis, 2006, 47(3): 396. doi: 10.1053/j.ajkd.2005.11.027 [5] YAMAMOTO R, NAGASAWA Y, SHOJI T, et al. Cigarette smoking and progression of IgA nephropathy[J]. Am J Kidney Dis, 2010, 56(2): 313. doi: 10.1053/j.ajkd.2010.02.351 [6] World Health Organization.Guidelines for controlling and monitoring the tobacco epidemic[S].Geneva: Tobacco or Health Programme, WHO, 1997. [7] ANDREOLI SP, BERGSTEIN JM. Treatment of severe IgA nephropathy in children[J]. Pediatr Ephrol, 1989, 3(3): 248. doi: 10.1007/BF00858524 [8] HASTINGS MC, MOLDOVEANU Z, JULIAN BA, et al. Galactose-deficient IgA1 in African Americans with IgA nephropathy: serum levels and heritability[J]. Clin J Am Soc Nephrol, 2010, 5: 2069. doi: 10.2215/CJN.03270410 [9] ROBERTS ISD.Pathology of IgA nephropathy[R].Nat Rev Nephrol, 2014. [10] XU HL, SUO JL, LIAN J. Cigarette smoking and risk of albuminuria in patients with type 2 diabetes: a systematic review and meta analysis of observational studies[J]. Int Urol Nephrol, 2018, 50(5): 911. doi: 10.1007/s11255-018-1825-x [11] GASTALDELLI A, FOLLI F, MAFFEI S. Impact of tobacco smoking on lipid metabolism, body weight and cardiometabolic risk[J]. Curr Pharm Des, 2010, 16(23): 2526. doi: 10.2174/138161210792062858 [12] KURUS M, UGRAS M, ESREFOGLU M. Effect of resveratrol on tubular damage and interstitial fibrosis in kidneys of rats exposed to cigarette smoke[J]. Toxic Health, 2009, 25(8): 539. doi: 10.1177/0748233709346755 [13] 张函, 章晓燕, 卢泽军, 等. 吸烟对IgA肾病(IgAN)患者肾功能和肾小管间质及血管病变的影响[J]. 复旦学报, 2014, 41(3): 315. doi: 10.3969/j.issn.1672-8467.2014.03.006 [14] YOON JC, BEOM JL, YONHEE K, et al. Smoking-related renal histologic injury in IgA nephropathy patients[J]. Yonsei Med J, 2016, 57(1): 209. doi: 10.3349/ymj.2016.57.1.209