ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: FR-PO126

Procalcitonin (PCT) Levels in Septic and Nonseptic Participants with AKI before and during Continuous Kidney Replacement Therapy (CKRT)

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Foulon, North, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States
  • Okamura, Kayo, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States
  • He, Zhibin, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States
  • Kennis, Matt Robert, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States
  • Colbert, James F., University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States
  • Faubel, Sarah, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States
Background

PCT is a 14.5 kDa protein and biomarker of bacterial infection. PCT is increased in ESKD and plasma levels decline after hemodialysis, suggesting clearance by the kidney and KRT. Herein, we measured plasma PCT in septic and non-septic patients with AKI and tested the hypothesis that PCT would be increased in AKI without sepsis and cleared by CKRT.

Methods

Plasma and effluent PCT were determined in septic and non-septic subjects with AKI that were selected from a prospective observational cohort of 126 patients who received CKRT at a single center. Plasma was collected prior to CKRT initiation, and plasma and effluent were collected on days 1, 2, and 3 of CKRT. Inclusion criteria for sepsis subjects were: 1) AKI without CKD, and 2) clinical diagnosis of sepsis and 2/2 positive blood cultures. Inclusion criteria for non-septic subjects were: 1) AKI without CKD, and 2) no clinical diagnosis of sepsis and no positive blood cultures. The sepsis cohort contained 9 patients, and the non-septic cohort contained 27 patients. 9 healthy control (HC) subjects with neither kidney disease nor sepsis were also studied.

Results

Plasma PCT was significantly increased in non-septic subjects with AKI vs. healthy controls. Plasma PCT was significantly increased in septic AKI subjects compared to non-septic (Figure 1). No significant difference existed in serum PCT of septic or non-septic AKI patients after 3 days of CKRT compared to pre-CKRT samples (Figure 2A and 2B). The average sieving coefficient for procalcitonin was 0.27 (Figure 3A). The average procalcitonin clearance was 7.05 L on day 1, 12.84 L on day 2, and 10.94 on day 3 of CKRT (Figure 3B).

Conclusion

Plasma PCT is significantly increased in non-septic patients with AKI suggesting that acute kidney function decline affects plasma PCT levels. Although some level of PCT clearance by CKRT was observed, changes in serum PCT were unpredictable during CKRT in both septic and non-septic patients. Our data suggest PCT results should be interpreted cautiously in patients with AKI prior to and during CKRT.