Abstract: FR-PO0405
Discrepancy Between Serum Creatinine and Serum Cystatin C in Precipitous AKI Due to Vancomycin
Session Information
- AKI: Biomarkers, Diagnostics, and Risk Prediction
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Li, Irene J., The University of Queensland Faculty of Medicine, Herston, Queensland, Australia
- Bendersky, Maggie, The University of Queensland Faculty of Medicine, Herston, Queensland, Australia
- Velez, Juan Carlos Q., Ochsner Health, New Orleans, Louisiana, United States
Group or Team Name
- Ochsner Nephrology
Background
Precipitous acute kidney injury (AKI) due to vancomycin (pV-AKI) is a distinct type of AKI manifested by an abrupt and steep rise in serum creatinine (sCr) shortly after exposure to high doses of IV vancomycin. The magnitude of the rise in sCr is often out of proportion to the observed clinical course, suggesting that the rise in sCr may be partially due to factors outside a true fall in GFR. To better examine kidney function changes during pV-AKI, simultaneous serum cystatin C (sCystC) determination can be used. Thus, we examined cases in which both sCr and sCystC were obtained during the course of pV-AKI.
Methods
We retrospectively examined records of patients seen in inpatient nephrology consultation for evaluation for AKI over an 8-year period. pV-AKI was defined as a rise in sCr ≥ 1.6 mg/dL within 24 +/- 2 hrs at any point during the course of a KDIGO AKI event. We then searched for concomitant measurement of sCystC during a pV-AKI event and analyzed the relationship between values.
Results
Among 63 cases of suspected pV-AKI, sCystC was measured in 12 (19%) cases. Those 12 cases were analyzed. Median age 53, 7 men, 4 women; 8 Black, 3 White, 1 Hispanic. In all pV-AKI cases, sCr and sCystC were simultaneously measured within the first 5 days of AKI (1 on day 1, 2 on day 2, 4 on day 3, 4 on day 4 and 1 on day 5). As expected, sCr and sCystC had a statistically significant positive correlation (r=0.514, p=0.04). However, the rise in sCr was noted to be steeper than that of sCystC as manifested by a regression sCr/sCystC slope of 0.98, significantly higher than the standard sCr/sCystC 0.80-0.90 slope. This was observed early in AKI despite the reported earlier rise in sCystC during AKI. Furthermore, for all 12 cases, a mean sCr of 6.36 mg/dL corresponded to a mean sCystC of 2.65 mg/dL, reflecting a mean 536% (280-1040%) increase in sCr from 1.0 mg/dL compared to a mean 163% (10-420%) increase in sCystC from 1.0 mg/L (p<0.0005).
Conclusion
The steep rise in pV-AKI is associated with a significantly less precipitous rise in sCystC, suggesting that the rise in sCr during pV-AKI is partially driven by non-GFR factors such as increased creatinine production and/or decreased tubular secretion of creatinine. To properly assess the clinical severity of a suspected case of pV-AKI, sCystC should be obtained.