Introduction

Acute kidney injury (AKI) is common in patients admitted to intensive care. Diagnosis of AKI relies on serum creatinine and urine flow. These have disadvantages of low specificity and sensitivity and a slow rate of change. Renal damage results in release of tubular enzymes into the urine. Measurement of urinary alpha glutathione S-transferase (αGST) and pi glutathione S-transferase (πGST) may indicate AKI more acutely and accurately than current methods of diagnosis.

Methods

Urine was collected from patients with a sepsis diagnosis 4 hourly over 48 hours. Urine was frozen, and urinary πGST and αGST measured. Fluid and vasopressor management was recorded, but managed independently. Serum creatinine was measured at 0, 24 and 48 hours. AKI was diagnosed using AKI Network criteria [1].

Results

We present the first 35 patients recruited, 20 were male, 15 female. Median patient age was 53 years. Median APACHE II score was 13. Median ICU length of stay was 9 days. ICU mortality was 14%, hospital mortality 23%. AKI was diagnosed in 26% of patients. Statistical significance was tested by Wilcoxon signed-rank test. Although the median πGST at 0 hours was elevated (11.8 μg/l (non-AKI) versus 22 μg/l (AKI)) this was not statistically significant between the two groups, P = 0.985. πGST did not demonstrate an increased urinary level in AKI versus non-AKI (median values 0.89 μg/l vs. 3.4 μg/l at 0 hours). See Figure 1.

Conclusion

A trend towards early expression of πGST was identifiable in this study. This may indicate early detection of AKI, which may help guide therapeutic interventions. πGST does not seem to be released as a biomarker using this sepsis model, suggesting a more specific distal tubular injury. Further work is required to determine levels of πGST in nonstressed kidneys.

References