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COMMENTARY
Year : 2014  |  Volume : 60  |  Issue : 2  |  Page : 160

Acute kidney injury biomarkers: Need to move from bench to bedside


Department of Nephrology, Seth Gordhandas Sunderdas Medical College and King Edward Memorial Hospital, Mumbai, Maharashtra, India

Date of Web Publication13-May-2014

Correspondence Address:
Dr. T E Jamale
Department of Nephrology, Seth Gordhandas Sunderdas Medical College and King Edward Memorial Hospital, Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Jamale T E, Hase N K. Acute kidney injury biomarkers: Need to move from bench to bedside. J Postgrad Med 2014;60:160

How to cite this URL:
Jamale T E, Hase N K. Acute kidney injury biomarkers: Need to move from bench to bedside. J Postgrad Med [serial online] 2014 [cited 2019 Nov 17];60:160. Available from: http://www.jpgmonline.com/text.asp?2014/60/2/160/132327


Contrast-induced acute kidney injury (CI-AKI) is an important cause of acute kidney injury (AKI) in hospital settings and is associated with prolonged hospital stay and adverse clinical outcomes. [1],[2] In this issue of the journal, Ebru et al. [3] have evaluated the utility of cystatin C-based criteria to diagnose CI-AKI as compared with the current practice of using serum creatinine. Cystatin C is recommended as a biomarker for screening and diagnosis of chronic kidney disease (CKD) in specific situations by Kidney Disease Improving Global Outcome (KDIGO) guidelines 2012. [4] However, its role in the diagnosis of AKI remains to be established. [5] A shorter half-life (and an earlier rise after insult), a predominantly extracellular distribution, and the fact that it is less affected by non-GFR factors such as muscle mass make it an attractive tool to assess renal function. [5] In their study of 121 patients, they found cystatin C to be more sensitive than creatinine and identified significantly more patients with CI-AKI. Despite a relatively low baseline risk (as assessed by Mehran score), lower dose of contrastused and a higher cutoff for cystatin C used for diagnosis (relative to a previous larger study), [6] the authors report a higher incidence of CI-AKI. This calls for better identification of at-risk population in cardiology settings, as heart disease itself is recognized as an important risk factor. [7] Also,noncontrast insults such as heart failure, atheroembolic disease, and drugs are not easy to differentiate. [8]

Putting this study in perspective, important issues regarding AKI biomarkers need discussion. Biomarkers are intended to identify patients with disease earlier so that early therapy can improve patient outcomes. Do AKI biomarkers serve this purpose? The last decade has witnessed an explosion of biomarkers to diagnose AKI earlier. Clinical relevance of earlier detection of AKI in most settings is debatable as therapy to alter natural history of tubular injury remains elusive. CI AKI and AKI in the settings of nephrotoxic chemotherapy may be important exceptions to this. After an early diagnosis one can expedite discharge from the hospital in the former and stop drugs in the latter setting with a potential to shorten hospital stay and prevent worsening of AKI. Unfortunately, this study could not evaluate whether cystatin C can help making such decision as authors measured it only after 24h. In addition to evaluating sensitivity, specificity, and net reclassification improvement, further studies involving biomarkers should include patient-centeredoutcomes such asdevelopment of clinically significant renal failure, duration of hospital stay, and the survival. Biomarker research needs to move from bench to bedside and further studies in settings of CI AKI will be an important step in that direction.

 
 :: References Top

1.Tepel M, Aspelin P, Lameire N. Contrast-induced nephropathy: A clinical and evidence-based approach. Circulation 2006;113:1799-806.  Back to cited text no. 1
    
2.Rudnick M, Feldman H. Contrast-induced nephropathy: What are the true clinical consequences? Clin J Am SocNephrol 2008;3:263-72.  Back to cited text no. 2
    
3.Ebru AE, Kilic A, Korkmaz FS, Seker R, Sasmaz H, Demirtas S, et al. Is Cystatýn-C is superýor to creatýnýne in the early diagnosýs of contrast-induced nephropathy?: A potential new býomarker for an old complication. J Postgrad Med 2014;60:135-40.  Back to cited text no. 3
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4.Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl 2013;3:1-150.  Back to cited text no. 4
    
5.Shlipak MG, Mattes MD, Peralta CA. Update on cystatin C: Incorporation into clinical practice. Am J Kidney Dis 2013;62:595-603.  Back to cited text no. 5
    
6.Briguori C, Visconti G, Rivera NV, Focaccio A, Golia B, Giannone R, et al. Cystatin C and contrast-induced acute kidney injury. Circulation 2010;121:2117-22.  Back to cited text no. 6
    
7.Mehran R, Aymong ED, Nikolsky E, Lasic Z, Iakovou I, Fahy M, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: Development and initial validation. J Am CollCardiol 2004;44:1393-9.  Back to cited text no. 7
    
8.Newhouse JH, Kho D, Rao QA, Starren J. Frequency of serum creatinine changes in the absence of iodinated contrast material: Implications for studies of contrast nephrotoxicity. AJR Am J Roentgenol 2008;191:376-82.  Back to cited text no. 8
    




 

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