Abstract

PurposeThe aim of this study was to assess the levels of selected markers in patients who underwent planned or emergency coronary angiography and to examine if they correlated with the occurrence of AKI.MethodsThe study included 52 patients who underwent planned or emergency coronary angiography and received contrast agent. Serum levels of markers (NGAL, L-FABP, KIM-1, IL-18) were analyzed in all patients using ELISA tests, at baseline, after 24 and 72 h from angiography.Results9.62% of patients developed CI-AKI. No significant differences were observed between markers levels in patients who developed CI-AKI and those who did not. After 24 h, serum levels of IL-18 were higher in patients with CI-AKI, however, this difference was on the verge of significance. Increase in serum NGAL, KIM-1 and IL-18 was observed after 24 h. Serum levels of biomarkers were insignificantly higher in group with CI-AKI. Significant changes in levels in time (baseline vs. 24 h vs. 72 h) were observed only for NGAL [157.9 (92.4–221.0) vs. 201.8 (156.5–299.9) vs. 118.5 (73.4–198.7); p < 0.0001]. No significant correlations were observed between the decrease in eGFR or the increase in creatinine and biomarkers level.ConclusionObtained results do not allow for the indication of efficient AKI biomarkers. Their further validation in large studies of CI-AKI patients is required.

Highlights

  • Acute kidney damage is a clinical syndrome that develops as a result of sudden impairment of kidney function [1]

  • The discrepancies in the incidence of contrast-induced AKI (CI-AKI) in many studies may be partly explained by the fact that small rises of serum creatinine are quite common in sick patients, even in those not receiving contrast [7, 8] and by the current use of lower doses of contrast, improved technologies as well as risk stratification of patients which enables the avoidance of contrast administration in the most risky patients

  • The Kidney Disease Improving Global Outcomes (KDIGO) working group suggests that AKI should be diagnosed when serum creatinine level has increased by at least 0.3 mg/dl (26.5 μmol/l) over the baseline value within 48 h after the exposure to contrast medium, or it has increased 1.5 times or more over the baseline value within 7 days after the exposure to contrast medium, or a urinary volume of less than 0.5 ml/ kg/h that persists for at least 6 h after exposure is observed [10]

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Summary

Introduction

Acute kidney damage is a clinical syndrome that develops as a result of sudden impairment of kidney function [1]. It is characterized by a wide spectrum of disorders ranging from a temporary increase in the concentration of biological markers, impaired renal function (elevated creatinine levels, decrease in GFR) to severe metabolic and clinical disorders,. The discrepancies in the incidence of CI-AKI in many studies may be partly explained by the fact that small rises of serum creatinine are quite common in sick patients, even in those not receiving contrast [7, 8] and by the current use of lower doses of contrast, improved technologies as well as risk stratification of patients which enables the avoidance of contrast administration in the most risky patients. Other causes for AKI such as atheroemboli, among others should be excluded [7]

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