B-type natriuretic Peptide and acute kidney injury: not yet ready for prime time*.

www.ccmjournal. org March 2014 • Volume 42 • Number 3 Acute myocardial infarction (AMI) is a common medical event that can result in dire clinical complications. Although the prevalence of coronary artery disease has declined, the prevalence of AMI still remains unchanged. More concerning is that after decades of improvements in mortality, we seem to have reached a plateau with respect to survival (1). One report recently published has demonstrated that mortality is unchanged despite improvement in processes of care, as defined by lower door to balloon time (2). One less well-described consequence of AMI is the occurrence of acute kidney injury (AKI). In a recent study, Fox et al (3) analyzed the prevalence and outcome of AKI in more than 59,000 patients presenting with AMI in 383 hospitals in the United States. The authors found that the prevalence of AKI was around 16% and its presence greatly increased the likelihood of death. These findings were confirmed by other reports (4). It is conceivable that timely appropriate prevention of AKI could reduce mortality, and for this reason, great efforts have been devoted to the prevention and medical treatment of AKI in patients presenting with acute coronary syndrome (ACS). However, currently there are no universally accepted effective preventative strategies. Why is that the case? An essential part of any successful intervention strategy starts with proper and accurate identification of AKI early enough in the course of the acute event in order to take measures to minimize and even potentially reverse kidney injury. Another important consideration is the ability to identify patients who are at greatest risk of developing severe AKI such that closer monitoring and swift intervention might be implemented. Current accepted practice relies on temporal changes in serum creatinine or urine output. Clinical criteria such as Risk, Injury, Failure, Loss and End-stage renal disease, Acute Kidney Injury Network, and Kidney Disease: Improving Global Outcomes have been developed and validated based on small changes in serum creatinine that occur within a time frame of 48 hours. Unfortunately, such a window may still be too long for effective early management, and the search for biomarkers that detect earlier renal injury remains an active area of great interest. What would an ideal biomarker look like? Naturally, an ideal biomarker would need to be highly sensitive (in order to avoid underdiagnosis) and specific (in order to avoid unnecessary additional testing or treatments). Because of the wide heterogeneity of mechanisms underlying causes of AKI, no single reliable biomarker has emerged. It may be that a panel of biomarkers, and perhaps more importantly, their variations over time and in proper clinical scenarios would be most useful (5, 6). The study by Moltraso et al (7) published in this issue of Critical Care Medicine adds some thoughtful findings. Moltraso et al (7) analyzed 639 patients with ACS (non–ST-elevation myocardial infarction and ST-elevation myocardial infarction [STEMI]) and analyzed the relationship between B-type natriuretic peptide (BNP) levels at admission and development of AKI. They found that of the 13% of patients in whom AKI was developed, BNP was not only significantly associated with AKI but also the degree of AKI risk increased in parallel with the absolute BNP level. In a previous study on patients presenting with STEMI, Jarai et al (8) showed that measuring BNP at admission enhanced the ability to identify patients at risk for developing AKI after percutaneous coronary intervention. Also in another study of patients undergoing elective cardiac surgery, preoperative BNP marginally improved classification for risk of AKI (9). Clearly, a correlation between admission BNP levels and risk of AKI has been previously established and confirmed by Moltraso et al (7). However, in terms of the capacity of BNP alone to predict AKI, the authors of the current study failed to demonstrate any improvement in risk prediction with BNP over other variables (age, left ventricular ejection fraction, estimated glomerular filtration rate, and type of ACS) previously shown to predict AKI risk. The question remains as to whether BNP represents a reliable early marker for AKI or simply a surrogate for other underlying cardiac or renal issues. Compared with clinical models, in both the study by Patel et al (9) and Moltraso et al (7), the application of BNP did not increase the area under the curve. Furthermore, patients with high BNP levels also had baseline lower ejection fraction, a variable that has already been shown to be associated with AKI. Also, the present study did not identify early treatment strategies used to manage the subjects on initial Copyright © 2013 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins DOI: 10.1097/CCM.0000000000000082 *See also p. 619.