Abstract
Although post exercise proteinuria has long been known, its exact pathophysiology is unclear Our objective was to determine whether long-term angiotensin converting enzyme (ACE) inhibition by different ACE inhibitors had an influence on post exercise proteinuria. We studied 14 patients who also had mild, chronic proteinuria caused by diabetes mellitus or chronic glomeruionephritis. We compared changes both in chronic (baseline) and post exercise proteinuria, during and after treatment with three different ACE inhibitors, with appropriate washout periods for the three drugs to all 14 patients. Proteinuria (mg/24 hours +/- SD), prior to the treatment was 682 +/- 92. Proteinuria after treatment for 30 days with benazepril was 464.4 ± 82.6 (p<0.001), with enalapril: 477.1 ± 105.5 (p<0.001), and captopril: 504.7 ± 100.1 (p<0.001). Proteinuria three days after discontinuing the treatment with benazepril was 532.4 ± 113.5, (p<0,01), with enalapril: 561.3 ± 128.5, (p<0.01), and with captopril: 620.8 ± 101,8, p = n.s. Post exercise proteinuria prior to treatment (mg/min. +/- SD) was. 138±0.32, vs. after a 30-day treatment period with benazepril: 0.81±0.19 (p<0.001), enalapril: 0.95±0.24, (p < 0.001), captopril: 1.09±0.27 (p<0.02). Post exercise proteinuria three days after discontinuing the treatment was (blood pressure already back to baseline): in case of benazepril: 1.26 +/- 0,36 (p=n.s), of enalapril: 1.17+/-0.46 (p=n.s), and of captopril: 1.34 +/- 0.41 (p=n.s.). We conclude that the renin-angiotensin system plays a significant role in the pathogenesis of post exercise proteinuria: the antiproteinuric effect of ACE inhibition in exercise-induced proteinuria seems to be associated chiefly with the hemodynamic changes due to these drugs, whereas in chronic proteinuria the antiproteinuric and antihypertensive effects are, at least partially, dissociated.