Abstract
The Pathophysiological Hypothesis of Kidney Damage during Intra-Abdominal Hypertension.
Highlights
Specialty section: This article was submitted to Clinical and Translational Physiology, a section of the journal Frontiers in Physiology
Pathophysiological mechanisms leading to acute kidney injury (AKI) during IAH are not completely known; evidence from the literature recognize the decrease in renal perfusion as the main factor responsible for development of AKI in this condition (De Waele et al, 2011)
An acute increase in intra-abdominal pressure (IAP) narrows renal arteries and veins, reduces renal blood flow, leading to the activation of autoregulatory mechanisms. These cause a vasodilation of afferent arterioles, ensuring glomerular filtration during the early stage of acute increase in IAP (Just, 2007)
Summary
Specialty section: This article was submitted to Clinical and Translational Physiology, a section of the journal Frontiers in Physiology. Pathophysiological mechanisms leading to AKI during IAH are not completely known; evidence from the literature recognize the decrease in renal perfusion as the main factor responsible for development of AKI in this condition (De Waele et al, 2011). Renal hypoperfusion might occur during an acute or progressive increase in IAP, mainly due to the reduction of both arterial inflow and venous outflow, leading to glomerular hemodynamic alterations.
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