The Renin–Angiotensin System, Not the Kinin–Kallikrein System, Affects Post-Exercise Proteinuria

Abstract

Background/Aims: Temporary proteinuria post-exercise is common and is caused predominantly by renal haemodynamic alterations. One reason is up-regulation of angiotensin II (Ang II) due to the reducing effect of angiotensin-converting enzyme (ACE) inhibitors. However, another, ignored, reason could be the kininase effect of ACE inhibition. This study investigated how ACE inhibition reduces post-exercise proteinuria: by either Ang II up-regulation inhibition or bradykinin elevation due to kininase activity inhibition. Methods: Our study included 10 volunteers, who completed 3 high-intensity exercise protocols involving cycling at 1-week intervals. The first protocol was a control arm, the second evaluated the effect of ACE inhibition and the third examined the effect of angiotensin type 1 receptor blockade. Upon application, both agents reduced systolic and diastolic blood pressure; however, there were no statistically significant ­differences. In addition, total protein, microalbumin and ­β₂-microglobulin excretion levels in urine specimens were analysed before, 30 min after and 120 min after the exercise protocols. Results: Total protein levels in urine samples were elevated in all 3 protocols after 30 min of high-intensity exercise, compared to baseline levels. However, both ACE inhibition and angiotensin type 1 receptor blockade suppressed total protein in the 30th min. In each protocol, total protein levels returned to the baseline after 120 min. Urinary microalbumin and β₂-microglobulin levels during the control protocol were significantly higher 30 min post-exercise; however, only angiotensin type 1 receptor blockade suppressed microalbumin levels. Conclusion: The results indicated Ang II up-regulation, not bradykinin elevation, plays a role in post-exercise proteinuria.

Biochemical Markers of Renal Hypoperfusion, Hemoconcentration, and Proteinuria after Extreme Physical Exercise

“…Reducing glomerular pressure by blocking the RAA (renin–angiotensin–aldosterone) system alleviates proteinuria, and is considered a fundamental part of nephroprotection in nephropathies with proteinuria [26,27]. During exercise, the filtration fraction increases due to a drop in RBF [12,28]. These changes are related to the activation of the sympathetic nervous system and the renin–angiotensin–aldosterone system [12,28].…”

“…During exercise, the filtration fraction increases due to a drop in RBF [12,28]. These changes are related to the activation of the sympathetic nervous system and the renin–angiotensin–aldosterone system [12,28]. Two recent studies have reported that changes in renal hemodynamics can contribute to albuminuria.…”

New insights about post‐exercise albuminuria in hypertensive patients

“…Glomerular pressure reduction through RAA system blockade alleviates albuminuria and is considered to exert a nephroprotective critical role in nephropathies with albuminuria . During physical activities, the filtration rate increases at least in part due to alterations in renal blood flow . These modifications are associated with activation of both the sympathetic nervous system and the RAA system .…”

“…During physical activities, the filtration rate increases at least in part due to alterations in renal blood flow . These modifications are associated with activation of both the sympathetic nervous system and the RAA system . Some data revealed that changes in renal hemodynamics could contribute to albuminuria .…”

“…These modifications are associated with activation of both the sympathetic nervous system and the RAA system . Some data revealed that changes in renal hemodynamics could contribute to albuminuria . A recent study described that in type 2 diabetic patients, who were mostly hypertensive (62%), light‐moderate exercise, similar to that of normal daily activity, induced albuminuria .…”