Changes in serum indoxyl sulfate levels after acute myocardial infarction and the correlation with kidney injury: an observational study

• Main Authors: Shuhei Watanabe, Hideki Fujii, Keiji Kono, Kentaro Watanabe, Shunsuke Goto, Susumu Sakamoto, Shinichi Nishi
• Format: Article
• Language: English
• Published: BMC 2019-07-01
• Series: Renal Replacement Therapy
• Subjects: Indoxyl sulfate; Acute myocardial infarction; Kidney injury
• Online Access: http://link.springer.com/article/10.1186/s41100-019-0225-8

Abstract Background 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. Methods In 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. Results Although 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. Conclusion This 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.