Skip to main content

The Value of Preventing Acute Kidney Injury for Cardiovascular Patients

By the bioMérieux Editors | Reading time: 3 min

PUBLICATION DATE: May 07, 2026

Acute kidney injury (AKI) continues to carry a significant burden on intensive care unit (ICU) patients and healthcare systems. This article summarizes the findings of our “The Value of Preventing Acute Kidney Injury” Dossier, including the current burden of AKI for hospitals, where current risk assessment practices fall short, and how VIDAS® NEPHROCHECK® [TIMP-2 · IGFBP-7] from bioMérieux is designed to fill in the gaps. 

To view the full Value Dossier findings, follow the link below. 

Get Complete Value Dossier

The Burden of Acute Kidney Injury

The percentage of hospitalizations in which AKI was diagnosed increased steadily from 2012 (16.8%) to 2021 (26.9%) before decreasing marginally, to 26.4%, in 2022.1 In the US, AKI is highly prevalent and an increasingly common complication 2–4 associated with longer hospital and ICU hospital length of stay (LoS)5,6 and an increased risk of in-hospital 7–10 and post-hospitalization mortality,11, 12 compared with no AKI. It is also associated with an increased risk of other in-hospital complications, dialysis use, and debilitating comorbidities.13

AKI is especially prevalent following cardiothoracic surgery, due to a variety of factors including low cardiac output, hemodilution (decreased carrying capacity of oxygen), administration of anti-hypertensive medications, and embolism.14-17

Why Traditional Indicators Delay AKI Risk Assessment 

Unlike other acute organ failures, AKI does not present with immediate or critical symptoms, making early diagnosis particularly challenging. Diagnosis and risk assessment is currently established through measurements of serum creatinine (SCr) and urine output (UO). However, this can result in delayed preventive treatment, ultimately putting patients at risk of harm.18,19

Functional markers including SCr and UO underperform in two ways:

1.       They lag behind the onset of kidney stress

Physiologically, AKI is defined by a decline in glomerular filtration rate (GFR). However, under stress the kidney can compensate for lost function and temporarily maintain overall renal GFR. During what is referred to as “subclinical AKI” up to 50% of kidney function may be lost before any changes occur in SCr or UO.20,21 Relying on these indicators therefore makes it more likely for AKI to have reached stage 2 or 3 before diagnosis, markedly increasing the risk of prolonged hospital stay, morbidity, and mortality.22

2.       They lack the necessary sensitivity and specificity

Neither SCr nor UO are specific to AKI or even to renal function. A number of potential confounders reduce the sensitivity and specificity of SCr and UO for AKI.23,24

VIDAS NEPHROCHECK: The Right Fit for AKI Risk Assessment

VIDAS NEPHROCHECK is an FDA-cleared risk assessment tool, indicated as an aid for assessing the risk of moderate or severe AKI in ICU patients with cardiovascular or respiratory compromise. It provides meaningful risk assessment for AKI as early as 4 hours after ICU admission, in contrast to SCr, which can take multiple days to reach a similar predictive capacity.24

The risk assessment is:

  • An easy and simple 46-minute urine test25
  • Specific to AKI as the TIMP-2 and IGFBP-7 biomarkers show no elevation with other common chronic and acute morbidities, such as sepsis25
  • Highly sensitive, identifying up 89.9% of patients who would develop AKI25

By permitting timely and specific AKI risk assessment—thereby significantly reducing the incidence of moderate-to severe AKI—VIDAS NEPHROCHECK has the potential to alleviate both the clinical and financial burden facing hospitals.

Want deeper insights? Download our The Value of Preventing Acute Kidney Injury Dossier below. 

Go to Full Dossier

References:

  1. United States Renal Data System. 2024 USRDS Annual Data Report: Epidemiology of kidney disease in the United States. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, 2024.
  2. Pavkov M, et al. Trends in Hospitalizations for Acute Kidney Injury — United States, 2000–2014. MMWR Morb Mortal Wkly Rep. 2018;67:289–293.
  3. Susantitaphong P, et al. World incidence of AKI: a meta-analysis. Clinical journal of the American Society of Nephrology:CJASN. 2013;8:1482-1493.
  4. Hoste EA BS, et al. Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med. 2015;8:1411-1423.
  5. Dasta JF, et al. Costs and outcomes of acute kidney injury (AKI) following cardiac surgery. Nephrol Dial Transplant. 2008;23:1970-4.
  6. Alshaikh HN, et al. Financial Impact of Acute Kidney Injury After Cardiac Operations in the United States. Ann Thorac Surg. 2018;105(2):469-475.
  7. Hobson C, et al. Cost and Mortality Associated With Postoperative Acute Kidney Injury. Ann Surg. 2015;261(6):1207-1214.
  8. Silver SA, et al. Cost of Acute Kidney Injury in Hospitalized Patients. J Hosp Med. 2017;12:70-76.
  9. Hu J, et al. Global Incidence and Outcomes of Adult Patients With Acute Kidney Injury After Cardiac Surgery: A Systematic Review and Meta-Analysis. J Cardiothorac Vasc Anesth. 2016;30(1):82-89.
  10. Machado MN, et al. Acute kidney injury based on KDIGO (Kidney Disease Improving Global Outcomes) criteria in patients with elevated baseline serum creatinine undergoing cardiac surgery. Rev Bras Cir Cardiovasc. 2014;29:299-307.
  11. Loef BG, et al. Immediate postoperative renal function deterioration in cardiac surgical patients predicts in-hospital mortality and long-term survival. J Am Soc Nephrol. 2005;16:195-200.
  12. Coca SG, et al. Long-term risk of mortality and other adverse outcomes after acute kidney injury: a systematic review and meta-analysis. Am J Kidney Dis. 2009;53:961-73.
  13. Doyle JF, Forni LG. Acute kidney injury: short-term and long-term effects. Critical Care. 2016;20:188.
  14. Brown, JK, et al. (2023). Adult Cardiac Surgery‑Associated Acute Kidney Injury: Joint Consensus Report. Journal of Cardiothoracic and Vascular Anesthesia. 37(9):1579–1590.
  15. Engelman DT, et al (2023). A Turnkey Order Set for Prevention of Cardiac Surgery–Associated Acute Kidney Injury. The Annals of Thoracic Surgery, 115(1), 11–15.
  16. Kamla CE, et al (2025). Kidney Injury Following Cardiac Surgery: A Review of Our Current Understanding. American Journal of Cardiovascular Drugs, 25, 337–348.
  17. Wang Y, et al (2017). Cardiac surgery-associated acute kidney injury: Risk factors, pathophysiology and treatment. Nature Reviews Nephrology. 13, 697–711.
  18. Ostermann M, et al. Acute kidney injury 2016: diagnosis and diagnostic workup. Crit Care. 2016;20(1):299. Published 2016 Sep 27.
  19. Moledina DG, et al. Phenotyping of Acute Kidney Injury: Beyond Serum Creatinine. Semin Nephrol. 2018;38(1):3-11.
  20. Ronco C, et al. Subclinical AKI is still AKI. Crit Care. (London, England) 2012;16:313-313.
  21. Sharma A, et al. Renal functional reserve and renal recovery after acute kidney injury. Nephron Clin Pract. 2014;127:94-100.
  22. Ronco C, et al. Acute kidney injury. Lancet. 2019;394:1949-1964.
  23. Bufkin, KB, et al. (2024). Review of the limitations of current biomarkers in acute kidney injury clinical practices. SAGE Open Medicine. 12:1–10.
  24. Meersch M, et al. Urinary TIMP-2 and IGFBP7 as early biomarkers of acute kidney injury and renal recovery following cardiac surgery. PLoS One. 2014 Mar 27;9(3):e93460. doi: 10.1371/journal.pone.0093460. PMID: 24675717; PMCID: PMC3968141.
  25. VIDAS® NEPHROCHECK® Package Insert 057209-01-2022-07.

SHARE THIS ARTICLE: