Can plasma TWEAK levels predict coronary slow flow in patients with chronic kidney disease?

Am J Med Sci. 2022 Nov;364(5):595-600. doi: 10.1016/j.amjms.2022.05.003. Epub 2022 May 8.

Abstract

Background: The tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is one of the inflammatory mediators contributing to the atherosclerotic process. TWEAK has been studied in patients with chronic kidney disease (CKD), and it has demonstrated that its level declines as estimated glomerular filtration rate (eGFR) decreases. Most studies have found that the decreased TWEAK levels were seen in atherosclerosis and associated with plaque calcification. The objective of this prospective study was to clarify any relationship between coronary slow-flow (CSF) and TWEAK levels in patients with CKD under conservative treatment.

Methods: This prospective study included 93 consecutive patients with CKD (mean creatinine level was 1.8±0.4 mg/dL) undergoing invasive coronary angiography (ICA) for any reason except for acute coronary syndromes from May 2019 to March 2020. A total of 93 patients were divided into two groups concerning having CSF (n=35) or no-CSF (n=58).

Results: Patients with CSF had higher TWEAK levels than those without CSF (695.2± 225.2 vs. 465.8±157.6, p<0.001). As the number of coronary arteries with slow flow increased, TWEAK levels increased statistically significantly (r:0.635/ p<0.001). Receiver operating characteristic (ROC) analysis showed that TWEAK levels of 516 pg/mL could predict CSF in patients with CKD.

Conclusions: Our study has shown that plasma TWEAK levels were an independent predictor for CSF in patients with CKD. In addition, our study has found that elevated TWEAK levels may not reflect the healthy arteries as it was hypothesized in the past.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Atherosclerosis* / blood
  • Atherosclerosis* / complications
  • Biomarkers / blood
  • Coronary Artery Disease* / blood
  • Coronary Artery Disease* / etiology
  • Creatinine / blood
  • Humans
  • Inflammation Mediators / blood
  • No-Reflow Phenomenon* / blood
  • No-Reflow Phenomenon* / etiology
  • Prospective Studies
  • Renal Insufficiency, Chronic* / blood
  • Renal Insufficiency, Chronic* / complications
  • Renal Insufficiency, Chronic* / therapy

Substances

  • Biomarkers
  • Creatinine
  • Inflammation Mediators
  • TNFSF12 protein, human