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Department of Anesthesiology, Duke University Medical Center, Box 3094 DUMC, Durham, NC 27710
(Email: staff002{at}mc.duke.edu).
If you have not already heard of the Acute Kidney Injury Network (AKIN), then let this commentary serve as your introduction. AKIN is a large and rapidly growing collaborative organization (www.akinet.org), primarily at this point involving critical care and nephrology societies (the Society of Cardiovascular Anesthesiologists will be the first perioperative organization to join). The goal of AKIN is to advance knowledge that will lead to evidence-based therapies for the treatment and prevention of acute kidney injury (AKI)
AKI is the term coined by AKIN to replace "acute renal injury." This change parallels a strategic approach to AKI investigation similar to "acute myocardial infarction" that has been so successful in improving patient care. AKIN is systematically outlining hurdles to progress—one of the earliest was an absence of a broadly accepted definition for AKI—and they have since proposed the widely accepted AKIN criteria based on creatinine rise or oliguria thresholds, or both. As troponin and creatine kinase-MB fraction have facilitated more timely interventions in the treatment of acute myocardial infarction than the traditional electrocardiogram Q wave, so now is the hope that early AKI biomarkers will revolutionize the field of AKI therapy relative to creatinine rise or dialysis.
The article by Haase and colleagues [1] nicely summarizes progress in the field of early AKI biomarker development. Although some new tools simply aim to substitute a more ideal creatinine-like substance for estimates of renal filtration (eg, cystatin C), most early markers relate to one of the three early consequences of AKI: tubular cell dysfunction, tubular cell damage, and the adaptive kidney stress response. The hope is that the prompt appearance of biomarkers will facilitate timely AKI risk identification, surveillance (ie, recognition of states such as prerenal azotemia), diagnosis, and prognosis. Strategic approaches such as focused multitest panels may improve the usefulness and precision of AKI biomarkers to address issues such as the timing of onset, grade of problem, and even the type of AKI, such as ischemic vs inflammatory.
Preliminary studies indicate that these goals are realistic; however, three caveats are relevant to AKI biomarker development and cardiac surgery. First, there is confusion surrounding the relationship of AKI biomarkers with end organ protection and outcome. We have learned from aprotinin that even when interventions produce favorable changes in hemostasis biomarkers and selected end organ function such as bleeding and transfusion, this should always be followed by trials confirming better overall outcome. Biomarker studies alone are rarely sufficient reason to change practice.
Second, oliguria, a criteria for AKI according to AKIN, is likely to prove much less associated with overall adverse outcome perioperatively compared with other settings.
Finally, a confusing but apparently benign interaction between lysine analogue antifibrinolytic agents (ie, 
-aminocaproic acid, tranexamic acid) and the proximal renal tubular transport mechanism that causes wasting into the urine of filtered microglobulins and other low-molecular-weight proteins can give a false impression of renal tubular injury. Proteinuria always occurs but also resolves within minutes of discontinuing these drugs.
The major hope is that improvements in monitoring with biomarkers will translate into better prevention, treatment, and outcome from AKI, something that has been disappointingly absent during the past half-century since perioperative acute renal failure was first described.
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