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Clinical Trial Summary

In the present study, 23 control individuals, 38 patients with systemic inflammatory response syndrome (SIRS), 20 septic and 45 sepsis-related acute kidney injury (AKI) patients were enrolled. Blood samples were collected from septic and sepsis-related AKI patients at the intensive care unit (ICU) at three time points (T1-3): T1: within 12 hours after admission; T2: second day morning of follow-up; T3: third day morning of follow-up. Sampling points for SIRS patients were the first (T1) and third (T3) postoperative morning. Exclusion criteria were patients under 18 years of age, unobtainable consent, end-stage renal disease requiring chronic dialysis or kidney transplantation and patients with malignancies needing palliative care. Not more than one sample (venous blood) was collected from control patients. Plasma presepsin levels were determined by an automated Point of Care instrument while serum gelsolin levels were measured using an automated immune turbidimetric assay. Plasma presepsin concentrations were expressed as pg/mL, while serum gelsolin levels were expressed as mg/L. Data were compared with laboratory and clinical parameters. Patients were categorized by the Sepsis-3 definitions and 14-day mortality data were investigated.


Clinical Trial Description

Presepsin is the 13-kDa soluble N-terminal fragment of the 55-kDa cluster of differentiation (CD) marker protein CD14, which is the receptor for lipopolysaccharide (LPS) and LPS-binding protein complexes. CD14 is a glycoprotein expressed mostly on the membrane surface of macrophages, monocytes and granulocytes which is released and degraded during inflammation after the recognition of pathogen-associated molecular patterns (PAMP), thus probably resulting in earlier elevation of plasma presepsin (PSEP) levels than the conventional sepsis biomarkers (C-reactive protein, procalcitonin). However, there is a concern that PSEP levels are affected by kidney function. Although its exact physiological activity is unclear, it is presumed that PSEP is filtered by the glomeruli, then reabsorbed and catabolized within proximal tubular cells. There is a growing body of evidence indicating increasing PSEP levels as kidney function decreases (e.g. during chronic kidney disease or sepsis-related AKI). Gelsolin (GSN) is a multifunctional protein existing in three different isoforms. Secreted or plasma GSN (MW = 83 kDa) is an essential component of the so-called extracellular actin scavenger system, therefore, decreasing serum GSN levels were reported in various clinical conditions (e.g. severe sepsis, multiple organ dysfunction syndrome (MODS), extensive trauma, acute liver failure, myocardial infarction). As albumin levels also tend to decrease in severe catabolic conditions, the simultaneous measurement of PSEP and GSN might yield additional information regarding the early diagnosis and severity of sepsis and sepsis-related AKI. Therefore, a new potential marker was investigated: Presepsin:gelsolin (PSEP:GSN) ratio. The main focuses of this study were investigating the kinetics of PSEP:GSN ratio and exploring the time course of PSEP levels in septic and sepsis-related AKI patients, as the early recognition of kidney injury - especially in sepsis - is essential in the aspect of therapy and survival. ;


Study Design


Related Conditions & MeSH terms


NCT number NCT05060679
Study type Observational
Source University of Pecs
Contact
Status Completed
Phase
Start date January 1, 2018
Completion date February 29, 2020

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