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尿酸水平对慢性肾脏病 3-4期IgA肾病预后影响的回顾性分析

Retrospective Analysis of the Effect of Uric Acid on the Prognosis of Immunoglobulin A Nephropathy With Stage 3-4 Chronic Kidney Disease

  • 摘要:
      目的  探究尿酸水平对慢性肾脏病(CKD)3-4期免疫球蛋白A肾病(IgAN)患者的临床病理及预后的影响。
      方法  回顾性收集2008年12月–2020年1月在西京医院经肾活检确诊的263例CKD 3-4期IgAN患者的临床和病理资料,根据空腹血尿酸水平是否>420 μmol/L将其分为高尿酸组(n=102)及尿酸正常组(n=161),比较两组的临床病理特征。以进展至终末期肾病或死亡为终点事件,通过Kaplan-Meier法比较两组患者的肾脏存活率,采用Cox和LASSO回归分析尿酸与预后的关系。
      结果  与尿酸正常组相比,高尿酸组男性及高血压病史的患者占比更多,血尿素氮(BUN)更高,估计肾小球滤过率(eGFR)、高密度脂蛋白(HDL)更低;在病理方面,高尿酸组患者肾小球硬化比例、系膜细胞增生、肾小管萎缩或肾间质纤维化较高,差异均有统计学意义(P<0.05)。Kaplan-Meier曲线显示两组肾脏生存率差异有统计学意义(P<0.0001); LASSO回归显示高尿酸是影响CKD 3-4期IgAN患者预后情况的危险因素,进一步的多因素Cox分析显示,与尿酸正常组相比,高尿酸组发生复合结局风险更高〔风险比(HR)=1.61,95%可信区间(CI):1.10~2.34〕。当尿酸作为连续性变量时,尿酸质量浓度每增加1 mg/dL,发生复合结局的HR增加1.18 (95%CI:1.08~1.29)。
      结论  高尿酸是CKD 3-4期IgAN患者肾脏预后不良的危险因素,降低尿酸水平可能有效改善高风险IgAN患者预后。

     

    Abstract:
      Objective  To investigate the effect of uric acid on the clinicopathological characteristics and prognosis of immunoglobulin A nephropathy (IgAN) in patients with stage 3-4 chronic kidney disease (CKD).
      Methods  The clinical and pathological data of 263 IgAN patients who had stage 3-4 CKD and who had confrimed diagosis through renal biopsy at the First Affiliated Hospital of Air Force Medical University between December 2008 and January 2020 were retrospectively collected. According to the levels of uric acid, the patients were divided into a hyperuricemia group (n=102) and a normal uric acid group (n=161), and the clinicopathological characteristics of the two groups were compared accordingly. With progression to end-stage renal disease or death as the endpoint event, the renal survival rate of the two groups was compared by the Kaplan-Meier method and the relationship between uric acid and the prognosis was analyzed by Cox regression and LASSO regression.
      Results  Compared with the normal uric acid group, the hyperuricemia group had a significantly higher proportion of male patients and patients with a history of hypertension, a significantly higher level of blood urea nitrogen, and lower levels of estimated glomerular filtration rate and high-density lipoprotein. In terms of pathology, patients in the hyperuricemia group had significantly higher proportion of glomerulosclerosis, higher mesangial hypercellularity, and higher tubular atrophy/interstitial fibrosis (P<0.05). Kaplan-Meier curve showed that there was a significant difference in renal survival rate between the two groups (P<0.0001). LASSO regression showed that high uric acid was a risk factor for the prognosis of IgAN patients with stage 3-4 CKD. Further multivariate Cox analysis showed that, compared with the normal uric acid group, the hyperuricemia group had a higher risk of incurring composite outcomes (hazard ratio HR=1.61, 95% confidence interval CI: 1.10-2.34). When uric acid was used as a continuous variable, the increase of 1 mg/dL in uric acid concentration was associated with an increased HR of 1.18 (95% CI: 1.08-1.29) for the composite outcome.
      Conclusion  High uric acid is a risk factor for poor renal prognosis in IgAN patients with stage 3-4 CKD and reducing uric acid levels may effectively improve the prognosis of high-risk IgAN patients.

     

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