Reátegui-Sokolova C, Ugarte-Gil Manuel F, Gamboa-Cárdenas Rocío V, Zevallos Francisco, Cucho-Venegas Jorge M, Alfaro-Lozano José L, Medina Mariela, Rodriguez-Bellido Zoila, Pastor-Asurza Cesar A, Alarcón Graciela S, Perich-Campos Risto A
Rheumatology Department, Hospital Nacional Guillermo Almenara Irigoyen, EsSalud, Av. Grau 800, La Victoria, Lima 13, Lima, Peru.
Universidad Científica del Sur, Lima, Peru.
Clin Rheumatol. 2017 Apr;36(4):845-852. doi: 10.1007/s10067-017-3538-4. Epub 2017 Jan 18.
This study aims to determine whether uric acid levels contribute to new renal damage in systemic lupus erythematosus (SLE) patients. This prospective study was conducted in consecutive patients seen since 2012. Patients had a baseline visit and follow-up visits every 6 months. Patients with ≥2 visits were included; those with end-stage renal disease (regardless of dialysis or transplantation) were excluded. Renal damage was ascertained using the SLICC/ACR damage index (SDI). Univariable and multivariable Cox-regression models were performed to determine the risk of new renal damage. Uric acid was included as a continuous and dichotomous (per receiving operating characteristic curve) variable. Multivariable models were adjusted for age at diagnosis, disease duration, socioeconomic status, SLEDAI, SDI, serum creatinine, baseline use of prednisone, antimalarials, and immunosuppressive drugs. One hundred and eighty-six patients were evaluated; their mean (SD) age at diagnosis was 36.8 (13.7) years; nearly all patients were mestizo. Disease duration was 7.7 (6.8) years. Follow-up time was 2.3 (1.1) years. The SLEDAI was 5.2 (4.3) and the SDI 0.8 (1.1). Uric acid levels were 4.5 (1.3) mg/dl. During follow-up, 16 (8.6%) patients developed at least one new point in the renal domain of the SDI. In multivariable analyses, uric acid levels (continuous and dichotomous) at baseline predicted the development of new renal damage (HR 3.21 (1.39-7.42), p 0.006; HR 18.28 (2.80-119.48), p 0.002; respectively). Higher uric acid levels contribute to the development of new renal damage in SLE patients independent of other well-known risk factors for such occurrence.
本研究旨在确定尿酸水平是否会导致系统性红斑狼疮（SLE）患者出现新的肾脏损害。这项前瞻性研究自2012年起对连续就诊的患者进行。患者进行了基线访视，并每6个月进行一次随访。纳入至少就诊2次的患者；排除终末期肾病患者（无论是否接受透析或移植）。使用SLICC/ACR损害指数（SDI）确定肾脏损害情况。采用单变量和多变量Cox回归模型来确定出现新肾脏损害的风险。尿酸作为连续变量和二分变量（根据受试者工作特征曲线）纳入分析。多变量模型对诊断时的年龄、病程、社会经济状况、SLE疾病活动指数（SLEDAI）、SDI、血清肌酐、基线时泼尼松、抗疟药和免疫抑制药物的使用情况进行了校正。共评估了186例患者；他们诊断时的平均（标准差）年龄为36.8（13.7）岁；几乎所有患者都是混血儿。病程为7.7（6.8）年。随访时间为2.3（1.1）年。SLEDAI为5.2（4.3），SDI为0.8（1.1）。尿酸水平为4.5（1.3）mg/dl。随访期间，16例（8.6%）患者在SDI的肾脏领域至少出现了一个新的评分点。在多变量分析中，基线时的尿酸水平（连续变量和二分变量）可预测新肾脏损害的发生（风险比分别为3.21（1.39 - 7.42），p = 0.006；18.28（2.80 - 119.48），p = 0.002）。较高的尿酸水平会导致SLE患者出现新的肾脏损害，且独立于其他已知的此类损害发生的危险因素。
