Skip to Main Content

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android. Learn more here!


Acute kidney injury (AKI) is a decline in renal function commonly seen in critically ill patients. During times of crisis, detection and treatment of AKI has become more complicated.


AKI has been associated with poor patient outcomes.1,2 Intrinsic risk factors include advanced age starting from 65 to 75 years of age, comorbid conditions including preexisting chronic kidney disease, diabetes mellitus, proteinuria, heart disease, chronic obstructive pulmonary disease, chronic liver disease, and peripheral vascular disease.1 The extrinsic or modifiable factors include sepsis, cardiac and vascular surgery, administration of iodinated contrast, traumas, burn injuries, medication and drug toxicities, and / or hypovolemia.1,2

The criteria for detection and staging of AKI continue to evolve. It involves changes with glomerular filtration through changes with serum creatinine and urine output. In 2004, the Acute Dialysis Quality Initiative (ADQI) introduced the Risk, Injury, Failure, Loss of kidney function, End stage renal disease classification (RIFLE).3 The Acute Kidney Injury Network (AKIN) proposed their classification in 2007.4 In 2012, with both validated initiatives possessing strengths and limitations, the Kidney Disease Improving Global Outcome (KDIGO) work group integrated the RIFLE and AKIN classifications to standardize the definition and severity of AKI.5 The KDIGO criteria was set forth to provide a single definition for purposes of clinical practice, research, and public health initiatives (Table 11-1).1


Despite all of this, only functional kidney impairment is being classified. The need for biomarkers to assess AKI risk stratification, diagnosis early kidney stress and subclinical acute kidney injury may allow for development of possible preventative and treatment options for AKI. Acute kidney stress referring to the pre-injury phase can possibly be identified through the expression of cell cycle arrest biomarkers.6 Subclinical AKI is an awareness of injury occurring before alterations in glomerular filtration. Promising serum and urinary biomarkers under investigation include neutrophil gelatinase-associated lipocalin (NGAL), cystatin-C (Cys-c), kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18), fatty acid binding proteins (FABPs), tissue inhibitor of metalloproteinases 2 (TIMP -2), insulin-like growth factor binding protein 7(IGFBP7), and endogenous ouabain (EO).7 The clinical utility of these biomarkers remains undetermined.

Renal functional reserve (RFR) is a concept of the kidney having the ability to increase ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.