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目的:观察影响2型糖尿病肾病(DN)患者尿微量白蛋白(MAU)进展和缓解的临床与病理因素,并分析其对肾小球滤过率(GFR)下降的影响。方法:纳入尿白蛋白定量30~300 mg/24h,血清肌酐≤109.62μmol/L,并愿意接受肾活检的2型DN患者61例。记录患者一般情况(基线年龄、糖尿病病程等)、临床指标(e GFR、血脂、血糖、尿白蛋白定量等)及病理指标(肾小球体积、系膜区面积百分比、基膜厚度、足细胞足突宽度等)。结果:61例患者中失访7例,MAU进展组22例(40.74%),MAU稳定组25例(46.30%),MAU转阴组7例(12.96%)。MAU转阴组患者基线尿白蛋白定量显著低于稳定组和进展组[(103.05±53.88)mg/24h vs(139.58±76.88)mg/24h vs(192.58±97.64)mg/24h,P=0.025],高密度脂蛋白水平显著高于稳定组和进展组[(1.38±0.34)mmol/L vs(0.94±0.23)mmol/L vs(1.04±0.37)mmol/L,P=0.006],足细胞裂孔膜分布密度显著高于稳定组和进展组[(1.01±0.21)个/μm vs(0.78±0.21)个/μm vs(0.58±0.30)个/μm,P=0.003]。多因素COX回归分析,显示足细胞裂孔膜分布密度(HR=0.029,P<0.001)和肾小球体积(HR=0.513,P=0.018)是MAU进展的独立影响因素;糖尿病病程(HR=0.925,P=0.012)、血尿酸(HR=1.012,P=0.034)、总胆固醇(HR=4.235,P=0.021)、ACEI/ARB使用(HR=311.451,P=0.006)是MAU转阴/缓解的独立影响因素。多因素Logistic回归分析显示,基线e GFR(HR=0.853,P=0.010)、血尿酸(HR=1.019,P=0.016)是e GFR下降的独立危险因素。结论:临床表现MAU的2型DN患者基线临床病理指标能够预测MAU进展与缓解,基线e GFR和血尿酸能够预测e GFR下降。
Objective: To observe the clinical and pathological factors that affect the progression and relief of urinary microalbumin (MAU) in patients with type 2 diabetic nephropathy (DN) and analyze its effect on glomerular filtration rate (GFR). Methods: Sixty-one patients with type 2 DN who accepted renal biopsy were enrolled in this study. The urinary albumin was quantified in 30-300 mg / 24h, serum creatinine was less than or equal to 109.62μmol / L. The clinical data (eGFR, blood lipid, blood glucose, urinary albumin, etc.) and pathological parameters (glomerular volume, area of mesangial area, basement membrane thickness, podocyte Foot width, etc.). Results: Of the 61 patients, 7 were lost to follow-up, 22 (40.74%) were in the MAU progression group, 25 (46.30%) in the MAU stabilization group and 7 (12.96%) in the MAU negative conversion group. Baseline urinary albumin quantitation was significantly lower in MAU-negative patients than in the stable and progression groups (103.05 ± 53.88 mg / 24h vs. 139.58 ± 76.88 mg / 24h vs 192.58 ± 97.64 mg / 24h, P = 0.025) , High density lipoprotein levels were significantly higher than those in the stable group and the progression group [(1.38 ± 0.34) mmol / L vs (0.94 ± 0.23) mmol / L vs (1.04 ± 0.37) mmol / L, P = 0.006] The membrane distribution density was significantly higher than that in the stable group and the progression group [(1.01 ± 0.21) / μm vs (0.78 ± 0.21) / μm vs (0.58 ± 0.30) /μm, P = 0.003]. Multivariate COX regression analysis showed that the distribution of podocyte perfusion (HR = 0.029, P <0.001) and glomerular volume (HR = 0.513, P = 0.018) were independent prognostic factors for MAU progression. The duration of diabetes mellitus (HR = 0.925 (HR = 311.451, P = 0.006) was the negative conversion of MAU (P = 0.012), serum uric acid (HR = 1.012, P = 0.034), total cholesterol Independent factors. Multivariate logistic regression analysis showed that baseline eGFR (HR = 0.853, P = 0.010) and serum uric acid (HR = 1.019, P = 0.016) were independent risk factors for eGFR decline. CONCLUSION: The baseline clinical and pathological parameters of type 2 DN patients with clinical manifestations of MAU can predict the progress and relief of MAU. The baseline e GFR and serum uric acid can predict the decrease of e GFR.