Cosenzi A, Carraro M, Sacerdote A, Franca G, Piemontesi A, Bocin E, Faccini L, Bellini G
Institute of Medical Pathology, University of Trieste, Italy.
Scand J Urol Nephrol. 1993;27(3):301-4. doi: 10.3109/00365599309180438.
Proteinuria after strenuous exercise is common in healthy subjects. The pathophysiologic mechanism of postexercise proteinuria (PEP) is not clear, although the phenomenon has long been known and many explanatory theories have been proposed. It is widely recognized that angiotensin II may increase filtration of protein through the glomerular membrane, and that its concentration in plasma increases during exercise. The aim of this study was to evaluate possible involvement of angiotensin II in the pathogenesis of PEP. Of 25 young volunteers who performed maximal aerobic exercise, eight showed PEP. The exercise was repeated after an interval of at least one week, now 90 minutes after administration of captopril (25 mg). Captopril did not affect the achieved work load of the maximal blood pressure and heart rate during the exercise, but PEP was not found. As it was possible to prevent PEP by administering an angiotensin-converting enzyme inhibitor, the study supports the theory that the renin angiotensin system is involved in the pathogenesis of PEP.
剧烈运动后出现蛋白尿在健康人群中很常见。尽管运动后蛋白尿（PEP）这一现象早已为人所知，且人们也提出了许多解释性理论，但PEP的病理生理机制仍不清楚。人们普遍认为，血管紧张素II可能会增加蛋白质通过肾小球膜的滤过，并且其在血浆中的浓度在运动期间会升高。本研究的目的是评估血管紧张素II在PEP发病机制中可能发挥的作用。在25名进行最大有氧运动的年轻志愿者中，有8人出现了PEP。在至少间隔一周后重复进行该运动，此次是在服用卡托普利（25毫克）90分钟后进行。卡托普利并未影响运动期间所达到的最大血压和心率的工作量，但未发现PEP。由于通过给予血管紧张素转换酶抑制剂有可能预防PEP，该研究支持肾素血管紧张素系统参与PEP发病机制的理论。
