Fig. 1
Diagram of renal hemodynamic mechanisms. a Reduction in mean arterial pressure (MAP) or cardiac output (CO), which determines renal preload, leads to decreased renal blood flow (RBF). This triggers an increase in renal arteriolar resistance (RRI), abnormally high in this context, resulting in a lowered glomerular filtration rate (GFR). This change adversely affects renal microcirculatory blood flow, contributing to AKI. b Increased central venous pressure (CVP), intra-abdominal pressures (IAP), or renal interstitial pressures (IRP) elevate renal venous pressure (RVP). c Discrepancies between renal macrocirculation and microcirculation may arise from various factors, including altered blood viscosity, endothelial dysfunction, increased leukocyte adhesion, glycocalyx degradation, and micro-thrombosis. d Enhanced intrarenal shunting can lead to reduced medullary tissue PO2, causing varying levels of tubular hypoxia. Conversely, a reduction in shunting effectiveness may also induce renal injury via a reactive oxygen species (ROS)-mediated pathway