Renal oxygenation, function and histopathology in an ovine model of heart failure undergoing cardiopulmonary bypass with 48 hours of recovery: a prospective, observational study*

Summary Introduction Acute kidney injury is common after cardiac surgery requiring cardiopulmonary bypass, yet preventive strategies are limited. Progress has been hindered by a lack of clinically relevant experimental models incorporating pre‐existing heart disease. This study aimed to evaluate the impact of heart failure on renal oxygenation and histopathological injury during and after cardiopulmonary bypass in a large animal model. Methods Heart failure was induced in 10 sheep (study group) via progressive coronary artery ligation; 10 healthy sheep served as controls (control group). We measured renal blood flow, renal function and renal cortical and medullary oxygenation before and after induction of anaesthesia, during 2 h of cardiopulmonary bypass and for 48 h postoperatively. Kidneys were collected at 48 h for histopathology. Results Cardiopulmonary bypass reduced renal blood flow (55%) and medullary oxygen tension (50%) in both groups (both p < 0.001). During the 48‐h recovery period, medullary oxygen tension remained low in the study group but normalised in the control group (mean (SD) 11 (11) vs. 31 (10) mmHg at 48 h, p = 0.01). Urine output was lower in the study group than in the control group over the 48‐h recovery period (mean (SD) 0.90 (0.54) vs. 2.24 (1.84) ml.kg ‐1 .h ‐1 at 48 h, p = 0.03). Histopathologically, the study group had a higher incidence of neutrophil infiltration (89% vs. 30%, p = 0.04), although the incidence of acute tubular necrosis, fibrosis and tubular casts did not differ significantly between groups. Discussion In this ovine model of heart failure, cardiopulmonary bypass led to persistent renal medullary hypoxia, oliguria and increased renal inflammation. These findings suggest that impaired renal medullary oxygenation and inflammation may drive cardiac surgery‐associated acute kidney injury and represent a key target for renoprotective strategies.