Plasma from Cardiac Surgery Patients Induces Endothelial and Tubular Epithelial Cell Damage: Potential Role in Acute Kidney Injury Development—A Preliminary Report

Cardiac surgery-associated acute kidney injury (CSA-AKI) is a frequent and severe complication of open-heart surgery. Although oxidative/inflammatory mechanisms are known to contribute to its pathophysiology, the circulating factors involved are poorly understood. In this preliminary investigation, we evaluated the effects of plasma from patients undergoing cardiac surgery on endothelial and renal tubular cells at anesthesia induction (T0) and 48 h after surgery (T1). Plasma levels of thiobarbituric acid-reactive substances (TBARSs), glutathione (GSH), and nitric oxide (NO) were measured in parallel. At T0, patient plasma showed increased TBARSs and reduced GSH and NO levels, consistent with oxidative imbalance, and induced cellular injury. In both cell types, plasma exposure reduced cell viability and mitochondrial membrane potential, while it increased oxidant release. Endothelial cells also showed decreased NO production, whereas renal tubular displayed increased apoptotic markers and reduced anti-aging factors. At T1, these alterations were further aggravated only in patients who developed CSA-AKI, whose plasma caused more severe endothelial and tubular damage. These findings support the presence of circulating injurious factors in cardiac surgery patient plasma that may contribute to CSA-AKI pathogenesis and help identify patients at risk before irreversible kidney damage develops.