Abstract

BackgroundKidney function after acute myocardial infarction (AMI) correlates with patient prognosis. Several studies reported the role that indoxyl sulfate (IS), a uremic toxin, plays in the progression of chronic kidney disease and cardiovascular diseases. This study aims at investigating the serum IS level changes after AMI and their correlation with kidney injury.MethodsIn this observational study, twenty consecutive patients with AMI who received percutaneous coronary intervention within 2 h after admission were enrolled. We measured serum IS levels on admission (day 1) and day 2–3 and evaluated their clinical characteristics. Further, we measured serum neutrophil gelatinase-associated lipocalin (NGAL) levels at admission as a marker of kidney injury.ResultsAlthough estimated glomerular filtration rate (eGFR) decreased at day 2–3 compared to that at day 1, serum IS levels at day 1 were rather higher than those at day 2–3. Further analysis only among patients with preserved kidney function revealed that serum IS levels at day 1 were significantly higher than those at day 2–3, despite a higher eGFR. Additionally, serum NGAL levels at admission were higher in these patients than in healthy subjects. Further, serum NGAL levels were significantly higher in patients with higher serum IS levels compared to those with lower IS levels.ConclusionThis study suggests that pathophysiological conditions in patients with AMI may elevate serum IS levels independent of kidney dysfunction and that IS may be one of the contributory factors related to kidney injury in AMI.

Highlights

  • Kidney function after acute myocardial infarction (AMI) correlates with patient prognosis

  • The results of this study revealed that serum indoxyl sulfate (IS) levels significantly decreased at day 2–3 compared to those at day 1, independent of the kidney function, and serum IS levels tended to correlate with serum neutrophil gelatinase-associated lipocalin (NGAL) levels at acute phase

  • We demonstrated that kidney injury biomarkers, such as NGAL, kidney injury molecule-1 (KIM-1), and liver-type fatty acidbinding protein (L-FABP), significantly decreased with the administration of AST-120, which reduces IS production

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Summary

Introduction

Kidney function after acute myocardial infarction (AMI) correlates with patient prognosis. Several studies reported the role that indoxyl sulfate (IS), a uremic toxin, plays in the progression of chronic kidney disease and cardiovascular diseases. This study aims at investigating the serum IS level changes after AMI and their correlation with kidney injury. Chronic kidney disease (CKD) is one of the crucial risk factors for cardiovascular disease (CVD); the association between CKD and CVD is termed as “cardiorenal syndrome.”. CKD is a risk factor for CVD, and in turn, CVD is a risk factor for CKD and acute kidney injury (AKI). The importance of kidney function preservation was recognized after CVD, the detailed mechanisms of “cardiorenal association” remain unclear. Research offers very little explanation of the mechanisms of CVD-caused kidney injury

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