Perez-Ruiz Fernando
Rheumatology Division, Hospital Universitario Cruces, University of the Basque Country, Bilbao, Vizcaya, Spain.
Rheumatol Ther. 2017 Dec;4(2):419-425. doi: 10.1007/s40744-017-0082-2. Epub 2017 Sep 27.
Gout is characterized by recurrent episodes of acute inflammation of joint structures, called gout flares, and flares are commonly treated with nonsteroidal anti-inflammatory drugs (NSAIDs). The objective of the study was to evaluate risk factors associated with acute kidney injury (AKI) attributed to NSAIDs in a cohort of patients who were exposed to NSAIDs to treat gout flares prior to urate-lowering therapy.
Retrospective analysis of a nested cohort of 983 gout patients in whom general variables (age, gender, renal function, ethanol intake, hypertension, hyperlipidemia, diabetes, vascular events, diuretic use) and also variables related to gout and severity of gout (serum urate levels, number for flares per year, presence of tophi, joint distribution, X-ray involvement, previous urate-lowering therapy) were available for analysis. Outcomes considered were loss of renal function attributed to NSAID prescription following the RIFLE classification for (risk, injury, and failure) for acute renal events. Variables associated with increased risk in Kaplan-Meier survival analysis were tested with multivariable Cox survival analysis, using time from onset of gout to the event as time exposed to NSAIDs.
Of 983 patients, 55 (5.6%) experienced AKI; the number of flares in the year previous to the renal event and polyarticular joint distribution were associated with higher risk of renal events. Other variables previously described in the literature, such as previous chronic renal disease, use of diuretics, and presence of previous vascular events, were also independently associated with increased risk of AKI. Interestingly, patients who had been previously prescribed allopurinol showed a lower risk of acute renal events.
In addition to classic risk factors, the number of flares and extensive joint distribution were associated with higher risk for renal injury in patients with gout, while previous prescription of allopurinol was associated with lower risk.
痛风的特征是关节结构反复出现急性炎症发作，称为痛风发作，通常使用非甾体抗炎药（NSAIDs）治疗发作。本研究的目的是评估在一组接受NSAIDs治疗痛风发作以进行降尿酸治疗的患者中，与NSAIDs所致急性肾损伤（AKI）相关的危险因素。
对983名痛风患者的嵌套队列进行回顾性分析，这些患者的一般变量（年龄、性别、肾功能、乙醇摄入量、高血压、高脂血症、糖尿病、血管事件、利尿剂使用情况）以及与痛风和痛风严重程度相关的变量（血清尿酸水平、每年发作次数、痛风石的存在、关节分布、X线受累情况、既往降尿酸治疗）均可用于分析。所考虑的结局是根据急性肾事件的RIFLE分类（风险、损伤和衰竭），归因于NSAID处方的肾功能丧失。在Kaplan-Meier生存分析中与风险增加相关的变量，使用从痛风发作到事件发生的时间作为暴露于NSAIDs的时间，通过多变量Cox生存分析进行检验。
983名患者中，55名（5.6%）发生了AKI；肾事件前一年的发作次数和多关节分布与肾事件风险较高相关。文献中先前描述的其他变量，如既往慢性肾病、利尿剂的使用以及既往血管事件的存在，也与AKI风险增加独立相关。有趣的是，先前开具过别嘌醇处方的患者急性肾事件风险较低。
除了经典危险因素外，发作次数和广泛的关节分布与痛风患者肾损伤风险较高相关，而先前开具别嘌醇处方与较低风险相关。
