Purpose of review: Renovascular disease (RVD) remains an important cause of hypertension and renal dysfunction. Given the failure of renal revascularization to provide consistent clinical benefit in the Cardiovascular Outcomes for Renal Artery Lesions trial among others, further research has underscored the need for mechanistically targeted interventions to improve renal outcomes in patients in RVD. This review discusses novel therapeutic approaches for RVD in the post-Cardiovascular Outcomes for Renal Artery Lesions era.
Recent findings: Emerging evidence indicates that renal inflammation, microvascular remodeling, and mitochondrial damage accelerate progression of renal injury and are important determinants of the response to revascularization. Experimental studies have identified interventions capable of ameliorating renal inflammation (e.g., cytokine inhibitors, mesenchymal stem cells), microvascular remodeling (proangiogenic interventions), and mitochondrial injury (mito-protective drugs), alone or combined with renal revascularization, to preserve the structure and function of the poststenotic kidney. Recent prospective pilot studies in patients with atherosclerotic RVD demonstrate the safety and feasibility of some of such interventions to protect the kidney.
Summary: Experimental studies and pilot clinical trials suggest that therapies targeting renal inflammation, microvascular remodeling, and mitochondrial damage have the potential to preserve the structure and function of the stenotic kidney. Further studies in larger cohorts are needed to confirm their renoprotective effects and clinical role in human RVD.