Elevated central venous pressure during cardiac surgery can lead to increased renal venous pressure, subsequently resulting in renal insufficiency. However, there is a lack of animal models available for studying this phenomenon. Therefore, we have successfully established a rat model of renal vascular congestion under cardiopulmonary bypass (CPB), providing a solid foundation for further investigations into the potential mechanisms underlying acute kidney injury (AKI) caused by renal hyperemia.

Ligation of the inferior vena cava between the renal veins of male SD rats resulted in hyperemia only in the left kidney. The left and right kidney control was formed under CPB and the left renal vein pressure was monitored. Six hours after operation, two kidneys were analyzed by molecular and histological techniques. The degree of tubulointerstitial injury, inflammatory infiltration, expression of inflammatory factors and molecular damage substances were evaluated in kidneys with and without venous stasis.

Histological examination showed that the left kidney, which received the intervention, exhibited congested renal tubules formed protein tubules and dilated. In addition, there were inflammatory cell infiltration in the interstitium and edema and necrosis in the local renal tubules. The right kidney, which did not receive the intervention, also showed similar changes, but the damage is mild. Immunohistochemistry showed that the expression of IL-6, IL-10 and KIM-1 in the left kidney was higher than that in the right kidney. Moreover, western blotting showed that the expression of KIM-1 and TNF-αin the left kidney was higher than that in the right kidney.

Renal vein congestion not only exacerbated structural damage to the kidneys in rats but also intensified the inflammatory response during CPB.