Abstract

Acute pancreatitis (AP) belongs to the commonest acute gastrointestinal conditions requiring hospitalization. Acute kidney injury (AKI) often complicates moderately severe and severe AP, leading to increased mortality. Among the laboratory markers proposed for early diagnosis of AKI, few have been studied in AP, including cystatin C and neutrophil gelatinase-associated lipocalin (NGAL). Beta-trace protein (BTP), a low-molecular-weight glycoprotein proposed as an early marker of decreased glomerular filtration, has never been studied in AP. We investigated the diagnostic usefulness of serum BTP for early diagnosis of AKI complicating AP in comparison to previously studied markers. BTP was measured in serum samples collected over the first three days of hospital stay from 73 adult patients admitted within 24 h of mild to severe AP. Thirteen patients (18%) developed AKI in the early phase of AP. Serum BTP was higher in patients who developed AKI, starting from the first day of hospitalization. Strong correlations were observed between BTP and serum cystatin C but not serum or urine NGAL. On admission, BTP positively correlated with endothelial dysfunction. The diagnostic usefulness of BTP for AKI was similar to cystatin C and lower than NGAL. Increased BTP is an early predictor of AKI complicating AP. However, it does not outperform cystatin C or NGAL.

Highlights

  • Beta-trace protein (BTP), known as lipocalin-type prostaglandin D2 synthase, is a monomeric 168-aminoacid protein belonging to the lipocalin family

  • Serum samples of 73 patients were available for the measurements of BTP, including 46 patients recruited in the Surgery Department, District Hospital in Sucha Beskidzka, Poland and 27 patients recruited in the Department of Surgery, Complex of Health Care Centers in Wadowice, Poland

  • Most laboratory markers proposed for the fast prognosis or diagnosis of Acute kidney injury (AKI) have not been studied in Acute pancreatitis (AP) [19]

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Summary

Introduction

Beta-trace protein (BTP), known as lipocalin-type prostaglandin D2 synthase, is a monomeric 168-aminoacid protein belonging to the lipocalin family. BTP was initially detected in cerebrovascular fluid and was shown to be synthesized in the central nervous system. BTP serves as a laboratory marker of cerebrovascular fluid leakage, and, for that purpose, robust automated measurement method has been developed and is available in routine laboratories [2,3]. Further studies revealed BTP is expressed in other organs, e.g., heart, lungs or kidneys, and the protein is present in biological fluids such as blood and urine [4]. The low molecular weight allows for free glomerular filtration of BTP present in blood. These characteristics enabled the use of BTP as a laboratory marker of renal filtration [5]

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