At the cellular level, reduced kidney perfusion in atherosclerotic renal arthery disease (ARVD), induces hypoxia, activation of the renin-angiotensin-aldosterone system (RAAS) and cytokine activation. Impaired blood f...At the cellular level, reduced kidney perfusion in atherosclerotic renal arthery disease (ARVD), induces hypoxia, activation of the renin-angiotensin-aldosterone system (RAAS) and cytokine activation. Impaired blood flow in the kidneys creates a microenvironment triggering significant cytokine production, contributing to vascular damage and endothelial disfunction. Interactions between cytokines and endothelial, glomerular, and tubular cells often result in increased vessel permeability, and fibrosis, and contribute to the development of chronic kidney disease (CKD). Molecules such as endothelins, prostaglandins, and nitric oxide play a crucial role at the molecular level. The imbalance between vasoconstrictor and vasodilator factors contributes to vascular dysfunction. Oxidative stress and inflammatory processes at the cellular level contribute to endothelial damage and structural changes in blood vessels. Mineralocorticoid receptor antagonists (MRAs) therapy in the context of ARVD holds promise in reducing fibrosis, promoting angiogenesis and enhancing overall outcomes in patients with this pathology. Recent data also indicates the antioxidative, anti-inflammatory, and antifibrotic effects of SGLT2 inhibitors. They reduce oxidative stress caused by hypoxic conditions and enhance renal perfusion, contributing to the preservation of cellular function. Studies employing Blood Oxygen Level-Dependent (BOLD) imaging have identified adaptations to reduced blood flow, volume, and glomerular filtration rate in post-stenotic kidneys that preserve oxygenation in the medulla and cortex during medical therapy. Data from the literature indicate that despite the partial recovery of renal hypoxia and restoration of blood flow after revascularization, inflammatory cytokines and injury biomarkers remain elevated, and the glomerular filtration rate (GFR) does not recover in ARVD. Restoration of vascular patency alone has failed to reverse tubulointerstitial damage and partially explains the limited clinical benefit of renal stenting. Considering these findings, BOLD MR imaging emerges as a technique capable of providing insights into the critical juncture of irreversibility in ARVD. However, further research is needed to monitor renal hypoxia following renal artery stenting and the inflammatory response over an extended period in conjunction with optimal therapy involving MRAs and SGLT2 agonists. The aim of research at the molecular level enables the identification of potential therapeutic modalities targeting specific molecular pathways, opening the door to innovative approaches in treating renovascular hypertension.展开更多
文摘At the cellular level, reduced kidney perfusion in atherosclerotic renal arthery disease (ARVD), induces hypoxia, activation of the renin-angiotensin-aldosterone system (RAAS) and cytokine activation. Impaired blood flow in the kidneys creates a microenvironment triggering significant cytokine production, contributing to vascular damage and endothelial disfunction. Interactions between cytokines and endothelial, glomerular, and tubular cells often result in increased vessel permeability, and fibrosis, and contribute to the development of chronic kidney disease (CKD). Molecules such as endothelins, prostaglandins, and nitric oxide play a crucial role at the molecular level. The imbalance between vasoconstrictor and vasodilator factors contributes to vascular dysfunction. Oxidative stress and inflammatory processes at the cellular level contribute to endothelial damage and structural changes in blood vessels. Mineralocorticoid receptor antagonists (MRAs) therapy in the context of ARVD holds promise in reducing fibrosis, promoting angiogenesis and enhancing overall outcomes in patients with this pathology. Recent data also indicates the antioxidative, anti-inflammatory, and antifibrotic effects of SGLT2 inhibitors. They reduce oxidative stress caused by hypoxic conditions and enhance renal perfusion, contributing to the preservation of cellular function. Studies employing Blood Oxygen Level-Dependent (BOLD) imaging have identified adaptations to reduced blood flow, volume, and glomerular filtration rate in post-stenotic kidneys that preserve oxygenation in the medulla and cortex during medical therapy. Data from the literature indicate that despite the partial recovery of renal hypoxia and restoration of blood flow after revascularization, inflammatory cytokines and injury biomarkers remain elevated, and the glomerular filtration rate (GFR) does not recover in ARVD. Restoration of vascular patency alone has failed to reverse tubulointerstitial damage and partially explains the limited clinical benefit of renal stenting. Considering these findings, BOLD MR imaging emerges as a technique capable of providing insights into the critical juncture of irreversibility in ARVD. However, further research is needed to monitor renal hypoxia following renal artery stenting and the inflammatory response over an extended period in conjunction with optimal therapy involving MRAs and SGLT2 agonists. The aim of research at the molecular level enables the identification of potential therapeutic modalities targeting specific molecular pathways, opening the door to innovative approaches in treating renovascular hypertension.
