Pons-Estel Guillermo J, Alarcón Graciela S, McGwin Gerald, Danila Maria I, Zhang Jie, Bastian Holly M, Reveille John D, Vilá Luis M
University of Alabama at Birmingham.
Arthritis Rheum. 2009 Jun 15;61(6):830-9. doi: 10.1002/art.24538.
To assess whether hydroxychloroquine can delay renal damage development in lupus nephritis patients.
Lupus nephritis patients (n = 256) from the LUpus in MInorities, NAture versus nurture study (n = 635), a multiethnic cohort of African Americans, Hispanics, and Caucasians, age > or =16 years with disease duration < or =5 years at baseline (T0) were studied. Renal damage was defined using the Systemic Lupus International Collaborating Clinics Damage Index (> or =1 of the following lasting at least 6 months: estimated/measured glomerular filtration rate <50%, 24-hour proteinuria > or =3.5 gm and/or end-stage renal disease, regardless of dialysis or transplantation). Patients with renal damage before T0 were excluded (n = 53). The association between hydroxychloroquine use and renal damage (as defined, or omitting proteinuria) was estimated using Cox proportional regression analyses adjusting for potential confounders. Kaplan-Meier survival curves based on hydroxychloroquine intake or the World Health Organization (WHO) class glomerulonephritis were also derived.
Sixty-three (31.0%) of the 203 patients included developed renal damage over a mean +/- SD disease duration of 5.2 +/- 3.5 years. The most frequent renal damage domain item was proteinuria. Patients who received hydroxychloroquine (79.3%) exhibited a lower frequency of WHO class IV glomerulonephritis, had lower disease activity, and received lower glucocorticoid doses than those who did not take hydroxychloroquine. After adjusting for confounders, hydroxychloroquine was protective of renal damage occurrence in full (hazard ratio [HR] 0.12, 95% confidence interval [95% CI] 0.02-0.97, P = 0.0464) and reduced (HR 0.29, 95% CI 0.13-0.68, P = 0.0043) models. Omitting proteinuria provided comparable results. The cumulative probability of renal damage occurrence was higher in those who did not take hydroxychloroquine and those classified as WHO class IV glomerulonephritis (P < 0.0001).
After adjusting for possible confounding factors, the protective effect of hydroxychloroquine in retarding renal damage occurrence in systemic lupus erythematosus is still evident.
评估羟氯喹能否延缓狼疮性肾炎患者肾脏损害的发展。
对来自“少数族裔狼疮：先天与后天研究”（共635例）中的狼疮性肾炎患者（n = 256例）进行研究，该研究为多民族队列研究，纳入了非裔美国人、西班牙裔和白种人，年龄≥16岁，基线时（T0）病程≤5年。肾脏损害采用系统性红斑狼疮国际协作临床损害指数进行定义（以下情况中至少1项持续至少6个月：估计/测量的肾小球滤过率<50%、24小时蛋白尿≥3.5克和/或终末期肾病，无论是否进行透析或移植）。排除T0之前已出现肾脏损害的患者（n = 53例）。使用Cox比例回归分析评估羟氯喹使用与肾脏损害（按定义或不包括蛋白尿）之间的关联，并对潜在混杂因素进行校正。还绘制了基于羟氯喹摄入情况或世界卫生组织（WHO）肾小球肾炎分类的Kaplan-Meier生存曲线。
在纳入研究的203例患者中，63例（31.0%）在平均±标准差为5.2±3.5年的病程中出现了肾脏损害。最常见的肾脏损害领域项目是蛋白尿。接受羟氯喹治疗的患者（79.3%）WHO IV级肾小球肾炎的发生率较低，疾病活动度较低，且糖皮质激素剂量低于未服用羟氯喹的患者。在对混杂因素进行校正后，在完整模型（风险比[HR] 0.12，95%置信区间[95%CI] 0.02 - 0.97，P = 0.0464）和简化模型（HR 0.29，95%CI 0.13 - 0.68，P = 0.0043）中，羟氯喹对肾脏损害的发生具有保护作用。不包括蛋白尿时得到了类似结果。未服用羟氯喹的患者和被分类为WHO IV级肾小球肾炎的患者发生肾脏损害的累积概率更高（P < 0.0001）。
在对可能的混杂因素进行校正后，羟氯喹在延缓系统性红斑狼疮患者肾脏损害发生方面的保护作用仍然明显。
