Procalcitonin levels in septic and nonseptic subjects with AKI and ESKD prior to and during continuous kidney replacement therapy (CKRT).

BACKGROUND: Procalcitonin is a 14.5 kDa protein used clinically as a marker of sepsis and therapeutic response to antibiotic therapy. However, its utility in critically ill patients with either acute kidney injury (AKI) or end-stage kidney disease (ESKD) who require continuous kidney replacement therapy (CKRT) is unknown. The aim of this study was to determine if plasma levels of procalcitonin could reliably distinguish septic from nonseptic status in patients with AKI or ESKD prior to or during CKRT. METHODS: Procalcitonin concentrations were measured in plasma of 41 critically ill septic or non-septic subjects with AKI or ESKD prior to CKRT (pre-CKRT) and on days 1, 2, and 3 of CKRT in this retrospective cohort study (n = 111 total plasma measurements). Continuous venovenous hemodialysis was the modality of CKRT in these patients. Sepsis status was stringently defined based on culture results. Effluent procalcitonin levels were ascertained on days 1, 2, and 3 of CKRT to assess the clearance of procalcitonin and effects on plasma levels. RESULTS: 92% (66/72) of the plasma procalcitonin measurements among nonseptic patients with either AKI or ESKD were ≥ 0.5 ng/mL (the diagnostic threshold beyond which bacterial infection is very likely). Prior to CKRT initiation, procalcitonin levels were (median (IQR), ng/mL) 5.6 (1.5-18.9) in nonseptic AKI and 58.1 (6.9-195.5) in septic AKI (P = 0.03) and were 3.3 (1.2-8.3) in nonseptic ESKD and 3.7 (1.4-209.8) in septic ESKD (P = 0.79). However, despite being significantly elevated in septic patients with AKI, substantial overlap among procalcitonin levels was present and ROC curve analysis found no cut point that could reliably separate septic from nonseptic patients. Effluent procalcitonin levels were consistently ~ 20% of plasma levels throughout the course of CKRT (i.e., sieving coefficient was 0.2) suggesting that clearance occurs during therapy. However, plasma procalcitonin levels did not significantly decline during CKRT in either AKI or ESKD. CONCLUSION: Procalcitonin levels are markedly elevated in nonseptic critically ill patients with either AKI or ESKD and do not effectively distinguish sepsis from nonseptic status prior to or during CKRT. We conclude that procalcitonin testing should be avoided in critically ill patients with kidney failure since results are nonspecific in this population.