Abstract
Acute kidney injury (AKI) is a syndrome that has progressed a great deal over the last 20 years. The decrease in urine output and the increase in classical renal biomarkers, such as blood urea nitrogen and serum creatinine, have largely been used as surrogate markers for decreased glomerular filtration rate (GFR), which defines AKI. However, using such markers of GFR as criteria for diagnosing AKI has several limits including the difficult diagnosis of non-organic AKI, also called “functional renal insufficiency” or “pre-renal insufficiency”. This situation is characterized by an oliguria and an increase in creatininemia as a consequence of a reduction in renal blood flow related to systemic haemodynamic abnormalities. In this situation, “renal insufficiency” seems rather inappropriate as kidney function is not impaired. On the contrary, the kidney delivers an appropriate response aiming to recover optimal systemic physiological haemodynamic conditions. Considering the kidney as insufficient is erroneous because this suggests that it does not work correctly, whereas the opposite is occurring, because the kidney is healthy even in a threatening situation. With current definitions of AKI, normalization of volaemia is needed before defining AKI in order to avoid this pitfall.
Highlights
Acute kidney injury (AKI) is a syndrome that has progressed a great deal over the last 20 years
The decrease in urine output and the increase in classical renal biomarkers, such as blood urea nitrogen (BUN) and serum creatinine (Scr), have largely been used as surrogate markers for decreased glomerular filtration rate (GFR), which defines AKI. Using such markers of GFR as criteria for diagnosing AKI has several limits including the difficult diagnosis of non-organic AKI, called “functional renal insufficiency” or “pre-renal insufficiency”
R1.1 Paediatrics—In paediatric patients, we suggest using the RIFLE classification modified for paediatric patients for diagnosing AKI: a decrease ≥25 % of estimated creatinine clearance or urine output
Summary
Acute kidney injury (AKI) is a syndrome that has progressed a great deal over the last 20 years. The decrease in urine output and the increase in classical renal biomarkers, such as blood urea nitrogen (BUN) and serum creatinine (Scr), have largely been used as surrogate markers for decreased glomerular filtration rate (GFR), which defines AKI. Using such markers of GFR as criteria for diagnosing AKI has several limits including the difficult diagnosis of non-organic AKI, called “functional renal insufficiency” or “pre-renal insufficiency” This situation is characterized by an oliguria and an increase in creatininemia as a consequence of a reduction in renal blood flow (RBF) related to systemic haemodynamic abnormalities. As in sepsis, major surgery and nephrotoxic agent administration These different notions of AKI and damage have emerged over the last few years, partly due to the discovery of new biomarkers for renal function that allow clinicians to accurately assess kidney damage, and renal dysfunction, before any subsequent change in the classical parameters of AKI.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
