Abstract
The pathophysiological mechanisms underlying CRS type 1 include renal hypoperfusion due to hypotension and low cardiac output, renal congestion, maladaptive activation of the renin–angiotensin–aldosterone and the sympathetic nervous system, and inflammation [1, 2]. Recent literature has shifted from low cardiac output to venous congestion (causing increased renal backpressure and compartment syndrome) as...
Full Text 
Sign-in/Register to access full text options
Sign-in/Register to access full text options 
Published version (
Free)
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
