Calvo-Alén J, De Cos M A, Rodríguez-Valverde V, Escallada R, Florez J, Arias M
Division of Rheumatology, Hospital Universitario M. de Valdecilla, School of Medicine, University of Cantabria, Santander, Spain.
J Rheumatol. 1994 Sep;21(9):1742-7.
To study the possible renal toxicity of longterm treatment with nonsteroidal antiinflammatory drugs (NSAID), in a population of patients with rheumatic diseases.
Comparative study of 104 patients treated for more than 2 years with NSAID and 123 healthy controls, nonusers of these drugs. After fasting during 12 h the following tests were performed in both groups: urinalysis, creatinine clearance, osmolar clearance, negative free water clearance, and urinary excretion of sodium.
In the patient group the urinary pH was higher than in the controls (5.9 +/- 0.7 versus 5.2 +/- 0.6 p < 0.05) and in addition, they had an impaired renal concentration capacity, as it is shown by a significant decreased urinary density (1018.6 +/- 4.7 vs 1026.3 +/- 5.4 in the controls p < 0.05), a decreased urinary osmolality (502.1 +/- 150.7 vs 661.6 +/- 157.6 mOsm/ml p < 0.001), a lower osmolar clearance (1.26 +/- 0.25 ml/min vs 1.83 +/- 0.4 ml/min p < 0.001) and an increased free water clearance (-0.21 +/- 0.40 ml/min vs -0.98 +/- 0.41 ml/min, p < 0.001). This renal impairment was related to the cumulative intake of NSAID:
The longterm treatment with NSAID is able to produce a subclinical renal dysfunction, consistent with the early stages of analgesic nephropathy.
研究长期使用非甾体抗炎药（NSAID）治疗对风湿性疾病患者人群可能产生的肾毒性。
对104例接受NSAID治疗超过2年的患者和123名未使用这些药物的健康对照者进行比较研究。两组患者均禁食12小时后，进行以下检查：尿液分析、肌酐清除率、渗透清除率、自由水清除率及尿钠排泄。
患者组尿液pH值高于对照组（5.9±0.7对5.2±0.6，p<0.05），此外，患者组肾脏浓缩功能受损，表现为尿比重显著降低（对照组为1026.3±5.4，患者组为1018.6±4.7，p<0.05）、尿渗透压降低（502.1±150.7对661.6±157.6mOsm/ml，p<0.001）、渗透清除率降低（1.26±0.25ml/min对1.83±0.4ml/min，p<0.001）以及自由水清除率增加（-0.21±0.40ml/min对-0.98±0.41ml/min，p<0.001）。这种肾功能损害与NSAID的累积摄入量有关。
长期使用NSAID能够导致亚临床肾功能障碍，与镇痛剂肾病的早期阶段相符。
