Within hospitals, acute kidney injury (AKI) is an often encountered, but poorly understood complication arising from major surgery, sepsis, infection, severe illness, circulatory shock and nephrotoxic drugs. In the spectrum of healthcare headaches, it is a triple-threat: common, costly and potentially catastrophic to patients-particularly those who are critically ill. 
Of the 5 million patients admitted to intensive care units (ICUs) in the United States each year, up to 50 percent will develop some form of AKI,1 which is associated with a ten-fold increase in hospital mortality rates.2 In terms of incidence, AKI is as common as myocardial infarction,3 and studies suggest that, in hospitalized patients, AKI may be twice as deadly.4
Once AKI takes hold, intervention is costly and time consuming, driving up length of stay and expense.2, 5 In the United States, the annual economic burden to the healthcare system for hospital-acquired AKI is estimated to exceed $10 billion,6 placing it among those complications associated with the highest in-hospital costs.
While early recognition and intervention are known to fend off irreversible injury associated with moderate to severe AKI, its lack of early signs and symptoms hinders detection, often delaying care. Data from the 2009 UK National Confidential Enquiry into Patient Outcomes and Death (NCEPOD) Adding Insult to Injury AKI study reported that, of admitted patients who died from hospital-acquired AKI, 31 percent had avoidable AKI and 43 percent had an unacceptable recognition delay.7
SEE ALSO: Getting the Word Out
Traditionally, the diagnostic approach to AKI has been grounded in the evaluation of kidney function accomplished through measurements of urine output and serum creatinine, well-known functional biomarkers. However, as Kellum and Chawla noted in a paper published recently in Nephrology Dialysis Transplantation, a change in function is not sufficient to define AKI as it is occurring, nor does a lack of change in function rule out injury.8 For a silent condition such as AKI, a diagnostic course employing risk assessment could prevent delays and aid clinicians in identifying and triaging vulnerable patients to potentially mitigate the consequences of AKI.
The Kidney Disease Improving Global Outcomes (KDIGO) Guideline for AKI and the American Society of Nephrology have each published guidelines or statements advocating research aimed at the identification of biomarkers that could be used to predict risk of AKI. KDIGO has also identified a number of clinical risk factors and susceptibilities associated with the condition.9, 10 But until recently, physicians have lacked a reliable means of assessing risk for those patients most vulnerable to moderate to severe AKI.3
Now, a growing body of evidence has emerged, supporting the efficacy of a new assay measuring the urinary concentration of two proteins, tissue inhibitor of metalloproteinase-2 (TIMP-2) and insulin-like growth factor binding protein-7 (IGFBP-7). The assay multiplies measurements of the two urinary biomarkers to derive a single quantitative test result (AKIRisk Score) that indicates risk of imminent AKI.
A single-use cartridge assays for both TIMP-2 and IGFBP-7 on a membrane test strip, employing a sandwich immunoassay technique. The test operator applies a fresh or thawed (i.e., previously frozen) clinical urine sample (mixed with labeled fluorescent conjugate) to the test cartridge, and then inserts it into a portable bench-top meter for incubation, reading and result calculation. The meter converts the fluorescent signal from each of the two immunoassays, TIMP-2 and IGFBP-7, into a single numerical result that is called the AKI RISK Score.11
