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Current Biomarkers under Investigation

David R. McIlroy, M.D., M.Clin.Epi., F.A.N.Z.C.A.

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† Associate Professor, Department of Anesthesiology, Columbia University College of Physicians and Surgeons, New York, New York.

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Anesthesiology April 2010, Vol. 112, 998–1004.

https://doi.org/10.1097/ALN.0b013e3181cded3f

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Bihorac A, Yavas S, Subbiah S, Hobson CE, Schold JD, Gabrielli A, Layon AJ, Segal MS: Long-term risk of mortality and acute kidney injury during hospitalization after major surgery. Ann Surg 2009; 249:851–8
Kheterpal S, Tremper KK, Heung M, Rosenberg AL, Englesbe M, Shanks AM, Campbell DA: Development and validation of an acute kidney injury risk index for patients undergoing general surgery: Results from a national data set. Anesthesiology 2009; 110:505–15
Xue JL, Daniels F, Star RA, Kimmel PL, Eggers PW, Molitoris BA, Himmelfarb J, Collins AJ: Incidence and mortality of acute renal failure in Medicare beneficiaries, 1992 to 2001. J Am Soc Nephrol 2006; 17:1135–42
Han W, Wagener G, Zhu Y, Wang S, Lee H: Urinary biomarkers in the early detection of acute kidney injury after cardiac surgery. Clin J Am Soc Nephrol 2009; 4:873–82
Wagener G, Gubitosa G, Wang S, Borregaard N, Kim M, Lee HT: Urinary neutrophil gelatinase-associated lipocalin and acute kidney injury after cardiac surgery. Am J Kidney Dis 2008; 52:425–33
Berl T: American Society of Nephrology Renal Research Report. J Am Soc Nephrol 2005; 16:1886–903
Hirose R, Xu F, Dang K, Liu T, Behrends M, Brakeman PR, Wiener-Kronish J, Niemann CU: Transient hyperglycemia affects the extent of ischemia-reperfusion induced renal injury in rats. Anesthesiology 2008; 108:402–14
Mishra J, Dent C, Tarabishi R, Mitsnefes MM, Ma Q, Kelly C, Ruff SM, Zahedi K, Shao M, Bean J, Mori K, Barasch J, Devarajan P: Neutrophil gelatinase-associated lipocalin (NGAL) as a biomarker for acute renal injury after cardiac surgery. Lancet 2005; 365:1231–8
Tuladhar SM, Puntmann VO, Soni M, Punjabi PP, Bogle RG: Rapid detection of acute kidney injury by plasma and urinary neutrophil gelatinase-associated lipocalin after cardiopulmonary bypass. J Cardiovasc Pharmacol 2009; 53:261–6
Koyner JL, Bennett MR, Worcester EM, Ma Q, Raman J, Jeevanandam V, Kasza KE, O'Connor MF, Konczal DJ, Trevino S, Devarajan P, Murray PT: Urinary cystatin C as an early biomarker of acute kidney injury following adult cardiothoracic surgery. Kidney Int 2008; 74:1059–69
Haase-Fielitz A, Bellomo R, Devarajan P, Story D, Matalanis G, Dragun D, Haase M: Novel and conventional serum biomarkers predicting acute kidney injury in adult cardiac surgery—a prospective cohort study. Crit Care Med 2009; 37:553–60
Makris K, Markou N, Evodia E, Dimopoulou E, Drakopoulos I, Ntetsika K, Rizos D, Baltopoulos G, Haliassos A: Urinary neutrophil gelatinase-associated lipocalin (NGAL) as an early marker of acute kidney injury in critically ill multiple trauma patients. Clin Chem Lab Med 2009; 47:79–82
Lebkowska U, Malyszko J, Lebkowska A, Koc-Zorawska E, Lebkowski W, Malyszko JS, Kowalewski R, Gacko M: Neutrophil gelatinase-associated lipocalin and cystatin C could predict renal outcome in patients undergoing kidney allograft transplantation: A prospective study. Transplant Proc 2009; 41:154–7
Knight EL, Verhave JC, Spiegelman D, Hillege HL, de Zeeuw D, Curhan GC, de Jong PE: Factors influencing serum cystatin C levels other than renal function and the impact on renal function measurement. Kidney Int 2004; 65:1416–21
Herget-Rosenthal S, Marggraf G, Husing J, Goring F, Pietruck F, Janssen O, Philipp T, Kribben A: Early detection of acute renal failure by serum cystatin C. Kidney Int 2004; 66:1115–22
Ahlstrom A, Tallgren M, Peltonen S, Pettila V: Evolution and predictive power of serum cystatin C in acute renal failure. Clin Nephrol 2004; 62:344–50
Parikh CR, Jani A, Melnikov VY, Faubel S, Edelstein CL: Urinary interleukin-18 is a marker of human acute tubular necrosis. Am J Kidney Dis 2004; 43:405–14
Parikh CR, Jani A, Mishra J, Ma Q, Kelly C, Barasch J, Edelstein CL, Devarajan P: Urine NGAL and IL-18 are predictive biomarkers for delayed graft function following kidney transplantation. Am J Transplant 2006; 6:1639–45
Parikh CR, Abraham E, Ancukiewicz M, Edelstein CL: Urine IL-18 is an early diagnostic marker for acute kidney injury and predicts mortality in the intensive care unit. J Am Soc Nephrol 2005; 16:3046–52
Washburn KK, Zappitelli M, Arikan AA, Loftis L, Yalavarthy R, Parikh CR, Edelstein CL, Goldstein SL: Urinary interleukin-18 is an acute kidney injury biomarker in critically ill children. Nephrol Dial Transplant 2008; 23:566–72
Ling W, Zhaohui N, Ben H, Leyi G, Jianping L, Huili D, Jiaqi Q: Urinary IL-18 and NGAL as early predictive biomarkers in contrast-induced nephropathy after coronary angiography. Nephron 2008; 108:176–81
Bulent Gul CB, Gullulu M, Oral B, Aydinlar A, Oz O, Budak F, Yilmaz Y, Yurtkuran M: Urinary IL-18: A marker of contrast-induced nephropathy following percutaneous coronary intervention? Clin Biochem 2008; 41:544–7
Parikh CR, Mishra J, Thiessen-Philbrook H, Dursun B, Ma Q, Kelly C, Dent C, Devarajan P, Edelstein CL: Urinary IL-18 is an early predictive biomarker of acute kidney injury after cardiac surgery. Kidney Int 2006; 70:199–203
Xin C, Yulong X, Yu C, Changchun C, Feng Z, Xinwei M: Urine neutrophil gelatinase-associated lipocalin and interleukin-18 predict acute kidney injury after cardiac surgery. Ren Fail 2008; 30:904–13
Haase M, Bellomo R, Story D, Davenport P, Haase-Fielitz A: Urinary interleukin-18 does not predict acute kidney injury after adult cardiac surgery: A prospective observational cohort study. Crit Care 2008; 12:R96
Han WK, Bailly V, Abichandani R, Thadhani R, Bonventre JV: Kidney Injury Molecule-1 (KIM-1): A novel biomarker for human renal proximal tubule injury. Kidney Int 2002; 62:237–44
Han WK, Waikar SS, Johnson A, Betensky RA, Dent CL, Devarajan P, Bonventre JV: Urinary biomarkers in the early diagnosis of acute kidney injury. Kidney Int 2008; 73:863–9
Liangos O, Perianayagam MC, Vaidya VS, Han WK, Wald R, Tighiouart H, MacKinnon RW, Li L, Balakrishnan VS, Pereira BJG, Bonventre JV, Jaber BL: Urinary N -acetyl-beta-(d)-glucosaminidase activity and kidney injury molecule-1 level are associated with adverse outcomes in acute renal failure. J Am Soc Nephrol 2007; 18:904–12
Hei Z, Li X, Shen N, Pang H, Zhou S, Guan J: Prognostic values of serum cystatin C and beta2 microglobulin, urinary beta2 microglobulin and N -acetyl-beta-d-glucosaminidase in early acute renal failure after liver transplantation. Chin Med J 2008; 121:1251–6
Wagener G, Gubitosa G, Wang S, Borregaard N, Kim M, Lee HT: Increased incidence of acute kidney injury with aprotinin use during cardiac surgery detected with urinary NGAL. Am J Nephrol 2008; 28:576–82
Rivera R, Antognini JF: Perioperative drug therapy in elderly patients. Anesthesiology 2009; 110:1176–81
Glasziou P, Irwig L, Deeks JJ: When should a new test become the current reference standard? Ann Intern Med 2008; 149:816–22
Waikar SS, Betensky RA, Bonventre JV: Creatinine as the gold standard for kidney injury biomarker studies? Nephrol Dial Transplant 2009; 24:3263–5
Bossuyt PM, Reitsma JB, Bruns DE, Gatsonis CA, Glasziou PP, Irwig LM, Moher D, Rennie D, de Vet HCW, Lijmer JG: The STARD statement for reporting studies of diagnostic accuracy: Explanation and elaboration. Ann Intern Med 2003; 138:W1–12
Haase M, Bellomo R, Devarajan P, Ma Q, Bennett M, Mockel M, Matalanis G, Dragun D, Haase-Fielitz A: Novel biomarkers early predict the severity of acute kidney injury after cardiac surgery in adults. Ann Thorac Surg 2009; 88:124–30

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David R. McIlroy, Gebhard Wagener, H. Thomas Lee, Bruno Riou; Biomarkers of Acute Kidney Injury : An Evolving Domain . Anesthesiology 2010; 112:998–1004 doi: https://doi.org/10.1097/ALN.0b013e3181cded3f
DESPITE more than half a century of investigation, acute kidney injury (AKI) remains a major healthcare issue in medicine today. Reported to occur in 1–32% of all hospital admissions and 10–90% of intensive care unit admissions, the wide variation reflects different criteria used to define AKI. However, independent of definition, a diagnosis of AKI is consistently associated with an increase in both short- and long-term morbidity and mortality. Even the mildest forms of AKI are independently associated with increased early as well as long-term mortality, the risk increasing as severity of renal injury increases. 1,2 Furthermore, the incidence of AKI is increasing. Based on a large administrative database study of hospital admissions from 1992 to 2001, Xue et al. 3 estimated an 11% increase per year in the incidence of AKI. However, of even greater concern is the failure to develop effective interventions to prevent or treat AKI, meaning that the current management remains directed toward supportive therapy while awaiting recovery of renal function.
A major impediment to developing effective therapeutic interventions to combat AKI has been the limited ability to accurately detect significant renal injury in a timely manner. Serum creatinine has been the predominant marker of renal function in clinical practice for more than half a century and its limitations are well documented. As a marker of renal function rather than injury, the nonlinear relationship between glomerular filtration rate and serum creatinine means glomerular filtration rate may decrease by more than 50% from normal before a significant rise in serum creatinine occurs, making creatinine insensitive to small but significant reductions in glomerular filtration rate. Furthermore, serum concentration is influenced by numerous nonrenal factors including age, race, gender, and muscle mass as well as factors such as drug metabolism, protein intake, perioperative fluid administration and hydration status. Consequently, it has proven difficult to define what change in creatinine constitutes significant AKI. The RIFLE criteria (an acronym of the sequentially graded Risk, Injury, Failure, Loss and End-stage classification system for AKI) and more recently the AKIN (Acute Kidney Injury Network classification of AKI) criteria represent attempts by international bodies of experts to standardize definitions and improve the understanding of the epidemiology of AKI. In validating these criteria, the significance of small changes in creatinine has been confirmed, emphasizing the enormous disease burden that AKI represents.
However, a further limitation in the use of creatinine to diagnose AKI is the inevitable delay between injury and the subsequent rise in serum creatinine. Although serum creatinine may begin to increase on postoperative day 1 after cardiac surgery, the majority of patients who develop AKI do not meet diagnostic criteria until postoperative day 2 or beyond. 4,5 Consequently, by the time serum creatinine can identify AKI, the inciting injury may be days old. Animal models of AKI consistently indicate that the window of opportunity for effective intervention to prevent or attenuate AKI is limited to within just a few hours of injury.
Acknowledging the inherent deficiencies of serum creatinine to diagnose AKI, the American Society of Nephrology in 2005 designated identification, characterization, and development of new AKI biomarkers as a key research area for the next 5 yr. 6 An ideal biomarker would identify patients at highest risk for AKI in a timely manner, thus allowing early and potentially effective intervention. Characteristics of the ideal AKI biomarker have been described and include early identification of injury, stratification according to injury severity, etiologic specificity for the injury, and providing valuable prognostic information ( table 1 ). However, the wide spectrum of pathophysiology leading to AKI makes it unlikely that any single biomarker will achieve all these aims. Several promising biomarkers of AKI have been identified, both in urine and plasma, and are currently the subject of ongoing studies defining their clinical utility ( fig. 1 ). However, the translational process from bench to bedside is complicated. Interpretation of novel biomarkers to detect minor but significant renal injury undetected by serum creatinine proved difficult in the 1990s as anesthesiologists investigated potential nephrotoxicity associated with sevoflurane. Although insensitive and slow to respond, creatinine remains the only marker validated against clinically relevant outcomes. Any potential replacement must therefore demonstrate the ability to identify clinically meaningful injury and be useful in guiding suitable interventions or other management decisions. Although the molecular pathways mediating renal injury are increasingly understood, with potential to quantify individual components of these pathways in the laboratory, 7 the focus of this clinical commentary is on biomarkers that reflect renal injury, which is frequently the result of multiple contemporaneous mechanisms in clinical practice.
Table 1. Characteristics of an Ideal Biomarker for Acute Kidney Injury
Fig. 1. Schematic representation of the predicted time course of change in biomarker levels for the detection of AKI after cardiac surgery in adults. Patterns of change represent ideal circumstances, which have not been consistently demonstrated in clinical studies. AKI = acute kidney injury; CPB = cardiopulmonary bypass; creatinine = serum creatinine; cystatin-C = serum cystatin-C; KIM-1 = urinary kidney injury molecule-1; NGAL = urinary neutrophil gelatinase–associated lipocalin.
Fig. 1. Schematic representation of the predicted time course of change in biomarker levels for the detection of AKI after cardiac surgery in adults. Patterns of change represent ideal circumstances, which have not been consistently demonstrated in clinical studies. AKI = acute kidney injury; CPB = cardiopulmonary bypass; creatinine = serum creatinine; cystatin-C = serum cystatin-C; KIM-1 = urinary kidney injury molecule-1; NGAL = urinary neutrophil gelatinase–associated lipocalin.
DNA microarray techniques searching for candidate biomarkers of AKI found neutrophil gelatinase-associated lipocalin (NGAL) as one of the maximally induced genes in a murine model of renal ischemia–reperfusion injury. A 25-kDa glycoprotein covalently bound to gelatinase, its resistance to proteolysis further
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