Crisp A J, Coughlan R J, Clark B, Mackintosh D, Panayi G S, Sweny P, Hopper J, Varghese Z
Clin Rheumatol. 1983 Sep;2(3):273-6. doi: 10.1007/BF02041402.
The urinary excretion of two proteins, B-2-microglobulin (beta 2M) and N-acetyl-B-D-glucosaminidase (NAG) was measured in 25 patients with rheumatoid arthritis (RA) on nonsteroidal anti-inflammatory drugs (NSAID). Although beta 2M excretion was normal NAG excretion was raised. As NAG excretion by a group of osteoarthritis patients receiving similar doses of NSAIDs was normal, it is concluded that rheumatoid disease per se may be associated with mild renal tubular dysfunction. Twelve of the above 25 patients were then given oral triethylphosphine-gold (auranofin) 6 mg daily and urinary beta 2M and NAG were measured after 6 months' treatment. Urinary excretion of beta 2M and NAG was also measured in 13 patients with RA established on intramuscular sodium aurothiomalate (MGST) and NSAIDs. Neither auranofin nor myocrisin were found to further significantly increase beta 2M and NAG excretion. These results suggest that gold compounds are not toxic to renal tubular epithelium.
对25名服用非甾体抗炎药（NSAID）的类风湿性关节炎（RA）患者的两种蛋白质，即β2-微球蛋白（β2M）和N-乙酰-β-D-氨基葡萄糖苷酶（NAG）的尿排泄情况进行了测定。尽管β2M排泄正常，但NAG排泄增加。由于一组接受相似剂量NSAIDs的骨关节炎患者的NAG排泄正常，因此得出结论，类风湿病本身可能与轻度肾小管功能障碍有关。上述25名患者中有12名随后每日口服6毫克三乙膦金（金诺芬），治疗6个月后测定尿β2M和NAG。还对13名已使用硫代苹果酸金钠（金硫葡糖）和NSAIDs的RA患者的尿β2M和NAG进行了测定。未发现金诺芬和硫代苹果酸金钠会进一步显著增加β2M和NAG的排泄。这些结果表明金化合物对肾小管上皮无毒性。
