Acute kidney injury (AKI) is an underrecognized and potentially catastrophic complication in hospitalized patients, with mortality rates in excess of 20%.1 It is a medical condition that is challenging to diagnose and manage; the earlier AKI can be diagnosed the better the outcomes for patients. However, medical intervention is often delayed owing to use of serum creatinine or urine volume for diagnosing AKI. These markers reflect renal function rather than the actual kidney injury and are insensitive parameters.

Over the past two decades, a plethora of biomarkers has been developed for the early diagnosis of AKI. An ideal biomarker should:

  • predict the severity of injury and need for renal replacement therapy.
  • aid in early diagnosis of acute tubular necrosis and in differentiating tubular injury from other causes of renal dysfunction.
  • help in determining the etiology and site of injury.
  • allow for monitoring the effect of an intervention.2

Neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), N-acetyl-β-D-glucosaminidase (NAG), interleukin-18 (IL-8), or cystatin C, have been put forward to aid in the early diagnosis of AKI. However, the utility of these biomarkers appears to be limited in the present clinical practice. DRG fielded a survey of 64 nephrologists and 35 critical care physicians practicing in the US to understand the underlying causes and challenges in managing AKI, including physicians’ perspectives on AKI diagnosis.

Source: Decision Resources Group. Current Treatment (US): Physician Insights – Acute Kidney Injury 2018.

Approximately, 75% of surveyed nephrologists and 90% of surveyed critical care physicians still use a combination of both serum creatinine and urine output for AKI diagnosis. The majority of the surveyed physicians also reported that glomerular filtration rate (GFR), and blood urea nitrogen (BUN) are highly important biomarkers in diagnosis and assessing the treatment efficacy for AKI. However, according to our survey, nephrologists and critical care physicians do not regularly use novel biomarkers like NGAL, KIM1, and NAG, IL-8, Cystatin C in their diagnostic work-up (see Figure). The low utility of novel biomarkers is likely due to sophisticated and expensive methods/assays required with these biomarkers that make them less preferred over the conventional biomarkers (serum creatinine and urine output) or simply that the novels tests may not be available.

Along with diagnosis, management of AKI is also a challenge. Currently, no pharmacotherapies are specifically approved for the prevention or treatment of AKI or to avoid the need for dialysis. For more information on the risk factors associated with AKI and the challenges in AKI management in the United States, see Decision Resources Group’s Current Treatment (US): Physician Insights –  Acute Kidney Injury 2018.


  1. Susantitaphong P, et al. World incidence of AKI: a meta-analysis. Clin J Am Soc Nephro. 2013;8:1482–1493.
  2. Parikh CR, et al. Biomarkers in Acute and Chronic Kidney Diseases. Skorecki K, et al. Brenner & Rector’s the kidney. 10th ed. Philadelphia: Elsevier, Inc.; 2016;1:926-938.

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