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  • Acute Kidney Injury (AKI) is a common medical condition that affects over 50% of ICU patients, and AKI requiring RRT has a mortality rate higher than MI, sepsis without AKI, or ARDS requiring mechanical ventilation in critically ill patients.

  • AKI does not occur in isolation, but instead has systemic effects on distant organs including the lung, heart, liver, brain, and immune system.

  • Sepsis-associated AKI is the most common cause of AKI in the ICU. Other causes include cardiorenal syndrome, cardiac surgery–associated AKI, hepatorenal syndrome, acute liver failure, intra-abdominal hypertension, and contrast-associated AKI.

  • Once AKI has occurred the management is supportive, including with RRT. Identifying patients at risk for developing AKI is therefore paramount for early implementation of preventive or therapeutic measures.

  • Novel biomarkers and functional tests are useful for diagnosing and prognosticating AKI. The former includes TIMP-2 and IGFBP7 and the latter includes the furosemide stress test (FST).


Acute kidney injury (AKI) is a common but serious medical condition in the intensive care unit (ICU) that is associated with significant increases in morbidity, mortality, and cost of care in both the short- and long-term. Increasingly, AKI is recognized not just as an organ-specific disease to be managed in isolation, but as a systemic disease that interacts and impacts the functioning of nearly every other organ. Because of its system-wide impact, AKI can be difficult to disentangle from other disease processes in critical illness in the heart, lungs, liver, immune system, and others. This chapter will define AKI and provide some background regarding its seriousness in the ICU and will then focus on some of the most common scenarios where AKI is encountered within critical illness. Some of the main takeaways of this chapter are as follows:

  1. AKI in the ICU is a common but serious condition that interacts with nearly every other organ system.

  2. There are no “mild” cases of AKI in the ICU.

  3. Because there are no effective pharmacologic treatments for AKI, it is important to accurately risk-stratify patients even before AKI develops in order to take appropriate preventative action.


AKI is characterized by a decline in glomerular filtration rate (GFR) over hours to days manifesting as either a rapid increase in serum creatinine, a decrease in urine output, or both.1,2 The term AKI is preferred over the formerly used acute renal failure as it refers to a spectrum of disease that is broader, including smaller but clinically significant changes in creatinine as well as severe cases requiring renal replacement therapy (RRT).3,4

While loss of GFR is the defining feature of AKI, GFR is difficult to directly measure in routine clinical practice.5 Because of this, surrogate measures of GFR, namely serum creatinine (SCr) levels and urine output, have been used to indicate changes in underlying GFR. Adding to the complexity, ...

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