Blockade of sympathetic nerve-derived signaling by renal denervation or adrenergic receptor blockade demonstrates therapeutic potential in preventing the progression of AKI to CKD and fibrogenesis.
Does blockade of sympathetic nerve-derived signaling by renal denervation or adrenergic receptor blockade prevent the progression of acute kidney injury to chronic kidney disease?
This review highlights the pathophysiological role of renal sympathetic overactivity in kidney disease progression and the therapeutic potential of renal denervation and adrenergic receptor blockade.
The kidney is innervated by afferent sensory and efferent sympathetic nerve fibers. Norepinephrine (NE) is the primary neurotransmitter for post-ganglionic sympathetic adrenergic nerves, and its signaling, regulated through adrenergic receptors (AR), modulates renal function and pathophysiology under disease conditions. Renal sympathetic overactivity and increased NE level are commonly seen in chronic kidney disease (CKD) and are critical factors in the progression of renal disease. Blockade of sympathetic nerve-derived signaling by renal denervation or AR blockade in clinical and experimental studies demonstrates that renal nerves and its downstream signaling contribute to progression of acute kidney injury (AKI) to CKD and fibrogenesis. This review summarizes our current knowledge of the role of renal sympathetic nerve and adrenergic receptors in AKI, AKI to CKD transition and CKDand provides new insights into the therapeutic potential of intervening in its signaling pathways.
Noh et al. (Fri,) conducted a review in Acute and Chronic Kidney Diseases. Renal denervation or adrenergic receptor blockade was evaluated. Blockade of sympathetic nerve-derived signaling by renal denervation or adrenergic receptor blockade demonstrates therapeutic potential in preventing the progression of AKI to CKD and fibrogenesis.