血红蛋白与IgA肾病患者肾小管萎缩/间质纤维化的关系

目的探讨IgA肾病(IgA nephropathy,IgAN)患者血红蛋白(Hb)水平与肾脏病理牛津分级中肾小管萎缩/间质纤维化(T)的关系。方法回顾性分析2010年1月1日至2015年12月31日在深圳市第二人民医院肾活检确诊为IgAN、同时有完整实验室及影像学资料的患者。将所有患者分为贫血组与非贫血组。采用Logistic回归分析确定Hb与肾小管萎缩/间质纤维化的关系;采用平滑曲线拟合分析Hb与肾小管萎缩/间质纤维化可能的曲线关系;采用受试者工作特征曲线(ROC)分析Hb对肾小管萎缩/间质纤维化的诊断价值。结果本研究共纳入IgAN患者630例,贫血组130例(20.63%),非贫血组500例(79.37%);两组间年龄差异无统计学意义,而性别差异有统计学意义(男性35.38%比53.80%,χ2=10.740,P<0.001)。与非贫血组相比,贫血组的患者肾小管萎缩/间质纤维化的比例和24 h尿蛋白量较高(χ2=62.586,P<0.001;Z=-6.082,P<0.001),估算的肾小球滤过率(eGFR)较低(t=7.126,P<0.001)。Logistic回归分析显示,高Hb水平为肾小管萎缩/间质纤维化发生风险减少的独立保护因素(OR=0.973,95%CI 0.958~0.987,P<0.001)。平滑曲线拟合分析显示Hb与肾小管萎缩/间质纤维化呈线性负相关。ROC曲线提示Hb诊断肾小管萎缩/间质纤维化的最佳临界值为120.5 g/L,即提示Hb>120.5 g/L时,肾小管萎缩/间质纤维化的程度可能降低。结论IgAN合并贫血的患者其肾小管萎缩/间质纤维化发生率较高。Hb>120.5 g/L可能减少肾小管萎缩/间质纤维化发生的风险。

Relationship between hemoglobin and renal tubular atrophy/interstitial fibrosis in patients with IgA nephropathy

Objective To clarify the relationship between the hemoglobin level and renal tubular atrophy/interstitial fibrosis (T) in the Oxford stage of renal pathology in IgA nephropathy (IgAN) patients. Methods Patients diagnosed with IgAN by renal biopsy from January 1st 2010 to December 31st 2015 in Shenzhen Second People's Hospital with complete laboratory and imaging data were retrospectively analyzed. Patients were divided into anemic group and non-anemic group. The relationship between hemoglobin level and renal tubular atrophy/interstitial fibrosis was determined by logistic regression analysis. The possible curve relationship between hemoglobin and renal tubular atrophy/interstitial fibrosis was analyzed by smooth curve fitting analysis. The diagnostic value of hemoglobin for renal tubular atrophy/interstitial fibrosis was analyzed by the receiver operating curve (ROC). Results A total of 630 patients with IgAN were included in this study, 130 patients in the anemia group (20.63%) and 500 patients in the non-anemia group (79.37%). There was no statistically significant difference in age between the two groups, but the difference of the gender was statistically significant (male 35.38% vs 53.80%, χ2=10.740, P＜0.001). Compared with the non-anemia group, the anemia group had a higher proportion of tubular atrophy/interstitial fibrosis ( χ2=62.586, P＜0.001), higher 24 h urinary protein quantification (Z=-6.082, P＜0.001), and lower eGFR (t=7.126, P＜0.001). Multivariate logistic regression analysis showed that increasing hemoglobin level was an independent protective factor for reducing the risk of renal tubular atrophy/interstitial fibrosis (OR=0.973, 95%CI 0.958-0.987, P＜0.001). Smooth curve fitting analysis showed that there was a linear negative correlation between hemoglobin and tubular atrophy/interstitial fibrosis. The ROC curve suggested that the best threshold of hemoglobin was 120.5 g/L when renal tubular atrophy/interstitial fibrosis occurred. That was, when hemoglobin was above 120.5 g/L, the severity level of renal tubular atrophy interstitial fibrosis might be reduced. Conclusion The incidence of renal tubular atrophy/ interstitial fibrosis is higher in IgAN patients with anemia, and hemoglobin＞120.5 g/L may reduce the risk of tubular atrophy/interstitial fibrosis.