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 ther...

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Vydané v:	Critical care (London, England) Ročník 29; číslo 1; s. 171
Hlavní autori:	Foulon, North, Haeger, Sarah M., Okamura, Kayo, He, Zhibin, Park, Bryan D., Budnick, Isadore M., Madison, David, Kennis, Matthew, Blaine, Rachel, Miyazaki, Makoto, Jalal, Diana I., Griffin, Benjamin R., Aftab, Muhammad, Colbert, James F., Faubel, Sarah
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	London BioMed Central 30.04.2025 BioMed Central Ltd Springer Nature B.V
Predmet:	Acute Kidney Injury - blood Acute Kidney Injury - therapy Aged Analysis Antibiotics Bacterial infections Biomarkers - analysis Biomarkers - blood Blood proteins Care and treatment Chronic kidney failure Cohort Studies Complications and side effects Continuous Renal Replacement Therapy - methods Creatinine Critical Care Medicine Critically ill Diagnosis Electronic health records Emergency Medicine Female Health aspects Hemodialysis Hemodynamics Humans Infection Intensive Kidney diseases Kidney Failure, Chronic - blood Kidney Failure, Chronic - therapy Male Medicine Medicine & Public Health Middle Aged Performance evaluation Plasma Population Procalcitonin - analysis Procalcitonin - blood Renal replacement therapy Retrospective Studies Risk factors Sepsis Sepsis - blood Sepsis - diagnosis United States Sepsis CKRT Procalcitonin ESKD AKI
ISSN:	1364-8535, 1466-609X, 1364-8535, 1466-609X, 1366-609X
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Abstract	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. Graphical abstract
AbstractList	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. 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. 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. 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. BackgroundProcalcitonin 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.MethodsProcalcitonin 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.Results92% (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.ConclusionProcalcitonin 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. 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. Graphical abstract 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 [greater than or equal to] 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. Graphical abstract Keywords: AKI, ESKD, CKRT, Procalcitonin, Sepsis 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. 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. 92% (66/72) of the plasma procalcitonin measurements among nonseptic patients with either AKI or ESKD were [greater than or equal to] 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. 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. 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.BACKGROUNDProcalcitonin 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.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.METHODSProcalcitonin 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.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.RESULTS92% (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.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.CONCLUSIONProcalcitonin 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.
ArticleNumber	171
Audience	Academic
Author	Griffin, Benjamin R. Budnick, Isadore M. Colbert, James F. Miyazaki, Makoto Foulon, North Kennis, Matthew Madison, David Blaine, Rachel Haeger, Sarah M. Park, Bryan D. Faubel, Sarah Aftab, Muhammad Okamura, Kayo He, Zhibin Jalal, Diana I.
Author_xml	– sequence: 1 givenname: North surname: Foulon fullname: Foulon, North organization: Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus – sequence: 2 givenname: Sarah M. surname: Haeger fullname: Haeger, Sarah M. organization: Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus – sequence: 3 givenname: Kayo surname: Okamura fullname: Okamura, Kayo organization: Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus – sequence: 4 givenname: Zhibin surname: He fullname: He, Zhibin organization: Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus – sequence: 5 givenname: Bryan D. surname: Park fullname: Park, Bryan D. organization: Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Medical Campus – sequence: 6 givenname: Isadore M. surname: Budnick fullname: Budnick, Isadore M. organization: Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Medical Campus – sequence: 7 givenname: David surname: Madison fullname: Madison, David organization: Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus – sequence: 8 givenname: Matthew surname: Kennis fullname: Kennis, Matthew organization: Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus – sequence: 9 givenname: Rachel surname: Blaine fullname: Blaine, Rachel organization: Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus – sequence: 10 givenname: Makoto surname: Miyazaki fullname: Miyazaki, Makoto organization: Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus – sequence: 11 givenname: Diana I. surname: Jalal fullname: Jalal, Diana I. organization: Department of Medicine, Division of Nephrology, University of Iowa Carver College of Medicine – sequence: 12 givenname: Benjamin R. surname: Griffin fullname: Griffin, Benjamin R. organization: Department of Medicine, Division of Nephrology, University of Iowa Carver College of Medicine – sequence: 13 givenname: Muhammad surname: Aftab fullname: Aftab, Muhammad organization: Department of Surgery, Division of Cardiothoracic Surgery, University of Colorado Anschutz Medical Campus – sequence: 14 givenname: James F. surname: Colbert fullname: Colbert, James F. organization: Department of Medicine, Division of Infectious Diseases, University of Colorado Anschutz Medical Campus – sequence: 15 givenname: Sarah surname: Faubel fullname: Faubel, Sarah email: Sarah.Faubel@cuanschutz.edu organization: Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus
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Snippet	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... 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... 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... BackgroundProcalcitonin is a 14.5 kDa protein used clinically as a marker of sepsis and therapeutic response to antibiotic therapy. However, its utility in... 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...
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SubjectTerms	Acute Kidney Injury - blood Acute Kidney Injury - therapy Aged Analysis Antibiotics Bacterial infections Biomarkers - analysis Biomarkers - blood Blood proteins Care and treatment Chronic kidney failure Cohort Studies Complications and side effects Continuous Renal Replacement Therapy - methods Creatinine Critical Care Medicine Critically ill Diagnosis Electronic health records Emergency Medicine Female Health aspects Hemodialysis Hemodynamics Humans Infection Intensive Kidney diseases Kidney Failure, Chronic - blood Kidney Failure, Chronic - therapy Male Medicine Medicine & Public Health Middle Aged Performance evaluation Plasma Population Procalcitonin - analysis Procalcitonin - blood Renal replacement therapy Retrospective Studies Risk factors Sepsis Sepsis - blood Sepsis - diagnosis
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Title	Procalcitonin levels in septic and nonseptic subjects with AKI and ESKD prior to and during continuous kidney replacement therapy (CKRT)
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