Concurrently, elevated renal venous pressure—stemming from right ventricular dysfunction or tricuspid regurgitation—and angiotensin II-mediated efferent arteriolar constriction reduce the glomerular filtration rate (GFR), fostering glomerulosclerosis and tubular atrophy, which are hallmarks of acute kidney disease (AKD) and chronic kidney disease (CKD).170–172 Inflammation and oxidative stress amplify this cascade; the ischemic myocardium releases proinflammatory cytokines (e.g., IL-6 and TNF-α) and ROS, damaging renal tubular epithelial cells and the endothelium. Here, AGT is linked to chronic kidney disease.