Autonomic imbalance and vascular injury in hypertensive chronic kidney disease: mechanisms and clinical potential of ultrasound-guided sympathetic blockade

Hypertensive Chronic Kidney Disease (CKD) constitutes a significant global health burden, characterized by a vicious cycle of hypertension and progressive renal decline. Autonomic imbalance, specifically sympathetic overactivity and parasympathetic withdrawal, is increasingly recognized as a central driver of this pathophysiology, interacting with traditional hemodynamic factors such as RAAS activation and volume overload. This review aims to elucidate the deep-seated mechanisms by which autonomic imbalance induces vascular injury and renal progression, and to evaluate the clinical potential of ultrasound-guided sympathetic blockade as a novel therapeutic strategy. We conducted a comprehensive narrative review of recent basic research and clinical evidence regarding the “Kidney-Brain-Vascular Axis” and neuromodulation therapies in the context of hypertensive CKD. The pathogenesis involves a maladaptive “Neuro-Immune-Vascular Axis.” Sympathetic overactivity not only induces hemodynamic stress but also disrupts the Th1/Th2 immune balance, accelerating vascular calcification and fibrosis. Ultrasound-guided sympathetic blockade offers a reversible, minimally invasive neuromodulation approach. Preliminary clinical evidence suggests it may lower blood pressure, improves vascular endothelial function, and potentially delays renal progression, particularly in patients with resistant hypertension, with a superior safety profile compared to renal denervation. Ultrasound-guided sympathetic blockade represents an emerging and investigational adjunct, constrained by the lack of large-scale randomized controlled trials and long-term outcome data.