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Abstract: PO0220

Interaction of Blood Urea Nitrogen and Tryptophan in Predicting Mortality in a Trauma-Induced Model

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

  • Singh, Pragya, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
  • Montemayor, Daniel, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
  • Pamreddy, Annapurna, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
  • Drel, Viktor, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
  • Kim, Jiwan John, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
  • Gao, Jingli, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
  • Ye, Hongping, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
  • Choi, Jae Hyek, United States Army Institute of Surgical Research, San Antonio, Texas, United States
  • Chung, Kevin K., United States Army Institute of Surgical Research, San Antonio, Texas, United States
  • Batchinsky, Andriy, United States Army Institute of Surgical Research, San Antonio, Texas, United States
  • Sharma, Kumar, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
Background

Multiple Organ Failure (MOF), often precipitated by Acute Respiratory Distress Syndrome (ARDS) brought on by trauma-induced injury, is a significant cause of death in military and civilian life. Furthermore, in ARDS, Acute Kidney Injury (AKI) is the most frequent organ failure affecting almost 50% of the patients, increasing the mortality rate. Therefore, understanding the molecular difference between survivors and non-survivors can significantly reduce the mortality burden.

Methods

A porcine MOF model (n =17) was developed using pulmonary contusion injury at Dr. Batchinsky's laboratory. In this model, n=10 are survivors, and n=7 are non-survivors with mortality at 3, 6, and 9 hours. Serum was employed for Amino acid metabolites using the Zip-Chip platform for mass spectrometry. A Cox proportional hazard analysis was employed to quantify the association of survival with the metabolite concentration. Serum blood urea nitrogen (BUN) was measured using the assay kit, and baseline BUN was correlated with baseline tryptophan level using a linear model.

Results

In survival analysis, survivors and non-survivors were partitioned by the mean metabolite concentration. The group with increased tryptophan concentration had a better chance of survival than the group with a reduction of tryptophan from the baseline. Furthermore, when associating the tryptophan level with the BUN, there is an opposite trend between the two groups. In the survivors, higher tryptophan is positively associated with increased BUN, whereas in the non-survivors, there is a negative correlation indicating that lower tryptophan coupled to high BUN increases the risk of mortality. Additionally, linear regression model showed a significant association of tryptophan and BUN with survivors and non-survivors.

Conclusion

Survival analysis indicated that a decrease in serum tryptophan level is a strong risk factor for mortality. Since tryptophan metabolism is associated with renal failure in AKI settings, we investigated serum tryptophan association with BUN. Non-survivors have a strong negative association of tryptophan with BUN, suggesting that combination of BUN and tryptophan could improve mortality risk prediction in early time-point in trauma-induced model.

Funding

  • Other U.S. Government Support