AKI Biomarkers www (Who, Where, When): You Cannot Treat What You Do Not Know (2014)

like www.biomarkers.something . Everything that is new in this area is online and reported on the Web in real time. However, I suggest the physician should look at the individual patient biomarker profile and develop a consequent diagnostic and therapeutic strategy that is personalized to that specific patient. In this area we must remove the barriers to early identification of patients at risk of developing AKI and possibly identify biomarkers useful for AKI risk assessment. The answers will come because the paradigm may shift and new biomarkers are probably capable of telling us the www: who should be monitored, where the damage is, and when treatment should start. Who. Recent studies have been published including discoveries of new molecules characteristic of specific structural damage and validation of their capacity to predict the development of AKI later on in the history of a critically ill patient [7–9] . In particular, urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2) are new biomarkers for AKI that were discovered in a cohort and validated in a large multicenter prospective study. They seem to perform better than existing markers with an AUC (area under the curve with 95% CI) higher than 0.8, especially when combined. [TIMP2] · [IGFBP7] also significantly improved risk stratification when added to a 9-variable clinical model. MAKE30 (major adverse kidney event within 30 days such as death, need for renal replacement therapy, or doubling of serum creatinine) increased sharply for [TIMP2] · [IGFBP7] >0.3 and doubled when values were >2.0 (ng/ml) 2 /1,000. One of the main questions in critical care nephrology is whether or why biomarkers of structural kidney damage are important in today’s clinical practice [1, 2] . The next question is whether biomarkers are potentially useful to guide early assessment of kidney damage and/or management of patients at risk for acute kidney injury (AKI) [3– 6] . There are several issues in the modern approach to AKI therapy and they can be summarized as follows. Which patient should be treated? What target should we consider important for therapy? How should we manage such complex patients? When should we begin the therapeutic strategy that has been proposed? What are the conditions for an appropriate intervention? What is the plan: prevent injury, avoid further injury, or mitigate present injury? What is the process of recovery? There are so many questions and so few answers. We must recognize that we cannot treat what we do not know. As we learn more about AKI, our therapeutic strategy will likely become an integrated process of primary prevention (this applies to populations and ethnic or geographical groups based on epidemiology and risk analyses), early diagnosis of the injury together with assessment of organ susceptibility, secondary prevention or mitigation of injury, and finally removal of current stressors or exposures leading to injury. The last factors are specific to the individual and suggest the need for a personalized approach. In this century, whenever a question is posed, scientists, students and the public at large rapidly ‘surf the Web’ to find an answer, possibly stumbling upon a page Published online: November 11, 2014