A NEW WAY TO DETECT ACUTE KIDNEY INJURY

Plain-language summary

Acute renal failure after cardiac surgery is a common postoperative complication, affecting approximately 20% of patients. It is associated with an increase in short-term mortality and an increase in hospital stay; but is also associated with an increase in long-term mortality of up to 30% at 5 years, even if renal function recovers upon discharge. Its origin is multifactorial: intraoperative hypoperfusion, including hemodynamic variations related to extracorporeal circulation or bleeding, postoperative hypoperfusion related to cardiogenic or vasoplegic shock, ischemia-reperfusion phenomena leading to cell lysis or inflammation at the tubular level, inflammation and oxidative stress related to extracorporeal circulation, and hemolysis are the main causes. Hydro-sodium overload and associated venous congestion is also one of the etiologies of acute renal failure in post-operative cardiac surgery and is associated with increased mortality. The proposed pathophysiological mechanism is based on the decrease in renal tissue perfusion pressure due to the increase in venous pressure. In the extreme, the increase in pressure in the renal capsule could lead to true renal ischemia due to engorgement. This renal congestion can be diagnosed based on clinical signs, biological signs (such as NT-pro-BNP) or by monitoring by central venous pressure (CVP). However, these statistical tools have low diagnostic performance, and new tools based on ultrasound and Doppler are being developed. Indeed, alterations in venous flow in the renal, suprahepatic and portal veins, reflecting the increase in pressures there, are associated with the onset of acute renal failure in post-operative cardiac surgery.

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