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Renal plexus

The renal plexus is a complex network of autonomic nerve fibers that provides innervation to the kidneys, comprising primarily sympathetic efferent and afferent components derived from the celiac plexus, intermesenteric plexus, and lumbar splanchnic nerves originating from spinal segments T9 to L2.^[1]^[2] These fibers travel along the renal arteries and veins, entering the kidney hilum to regulate key physiological processes such as vasoconstriction, sodium reabsorption, renin release via the juxtaglomerular apparatus, and nociceptive signaling.^[1]^[3] Lacking direct parasympathetic innervation, it is predominantly sympathetic in nature—with postganglionic adrenergic neurons releasing norepinephrine to act on α1- and β1-adrenoceptors—though evidence for indirect parasympathetic contributions remains minimal.^[2]^[1] The renal plexus arises from preganglionic sympathetic fibers in the intermediolateral column of the thoracic and upper lumbar spinal cord (T9–T12, occasionally extending to L2), which synapse in nearby prevertebral ganglia such as the celiac and aorticorenal ganglia before forming postganglionic fibers.^[2]^[3] Afferent fibers within the plexus convey sensory information, including pain from renal capsule distension or ischemia, projecting to central structures like the hypothalamus, brainstem, and subfornical organ to influence systemic responses such as blood pressure modulation.^[1] Efferent sympathetic innervation is densest at the corticomedullary junction, targeting renal arterioles (interlobar, arcuate, and interlobular), glomerular structures, and tubular segments—particularly the proximal tubule and thick ascending limb—to control vascular tone, glomerular filtration rate, and electrolyte handling.^[2] Neurotransmitters involved include norepinephrine as the primary mediator, often co-released with neuropeptide Y and ATP, though the latter's roles in renal function are less defined.^[2] Anatomically, the renal plexus is positioned retroperitoneally along the renal vessels, closely associated with the aorta and inferior vena cava, and it extends minor branches to the adrenal glands and upper ureter.^[3]^[1] This innervation integrates with the broader abdominal autonomic system, receiving inputs from the least thoracic splanchnic nerve (T12) and intermesenteric nerves, ensuring coordinated regulation of renal hemodynamics and the renin-angiotensin-aldosterone system in response to systemic demands like volume depletion or hypertension.^[3]^[2] Disruptions in renal plexus activity, such as through denervation procedures, have therapeutic implications for conditions like resistant hypertension, underscoring its critical role in cardiovascular homeostasis.^[1]

Anatomy

Location

The renal plexus is a bilateral network of autonomic nerves situated along the renal arteries, extending from their origin at the abdominal aorta to the renal hilum.^[4] It is closely associated with the retroperitoneal positioning of the kidneys, accompanying the arteries bilaterally as they course posteriorly to the respective renal veins.^[1] This plexus forms a perivascular meshwork surrounding both the renal artery and vein, with its fibers entering the kidney at the hilum alongside the ureter.^[5] From there, branches distribute into the renal pelvis, calyces, and parenchyma to reach the renal vasculature and structures.^[5] The renal plexus arises in continuity with broader autonomic networks, including the celiac and aorticorenal plexuses.^[1]

Formation and components

The renal plexus is formed by 15–20 filaments originating from the celiac ganglia and plexus, the aorticorenal ganglia, the lower thoracic splanchnic nerves (T10–T12), the first lumbar splanchnic nerve, and the aortic plexus.^[6] ^[1] Small ganglia develop along these contributing nerves, contributing to the plexus's networked structure.^[6] The plexus's branches supply the kidney directly, targeting its vessels, glomeruli, and tubules, while also extending to the upper ureter via the ureteric plexus.^[6] ^[2] Additional filaments connect to the spermatic or ovarian plexus and reach the fundus of the uterus.^[6] Microscopically, the renal plexus comprises a mixture of myelinated and unmyelinated fibers, predominantly the latter (approximately 96% in studied models), with fiber diameters varying from 0.5 to 10 μm—unmyelinated fibers averaging 1.3 μm and myelinated fibers around 3.1 μm, though some myelinated fibers exceed 5 μm.^[2] ^[7] ^[8]

Innervation

Sympathetic fibers

The sympathetic fibers of the renal plexus provide efferent innervation to the kidney, originating from preganglionic neurons in the intermediolateral cell column of the thoracolumbar spinal cord, specifically segments T9 to L2.^[2] These preganglionic fibers exit via the ventral roots and travel through white rami communicantes to synapse primarily in the celiac and aorticorenal ganglia, as well as other prevertebral sympathetic ganglia.^[1] Postganglionic fibers then emerge from these ganglia and join the renal plexus, which forms around the renal artery and vein before entering the kidney at the hilum.^[2] These postganglionic fibers innervate key renal structures, including the renal arterioles (interlobar, arcuate, interlobular, and glomerular afferent/efferent), juxtaglomerular cells, and segments of the nephron such as the proximal tubule, thick ascending limb, distal tubule, and collecting duct.^[2] The innervation supports vascular tone regulation and tubular function, with fibers distributing along the vascular tree and into the renal parenchyma.^[1] The sympathetic fibers are predominantly noradrenergic, releasing norepinephrine that acts on adrenergic receptors to elicit physiological responses. Activation of alpha-1 adrenoceptors on vascular smooth muscle induces vasoconstriction, reducing renal blood flow, while beta-1 adrenoceptors on juxtaglomerular cells stimulate renin release, contributing to the activation of the renin-angiotensin-aldosterone system.^[2] The density of these fibers is highest in the renal cortex, particularly around afferent arterioles, with a notable concentration at the corticomedullary border and decreasing toward the inner medulla.^[2]

Parasympathetic and sensory fibers

The renal plexus receives sparse parasympathetic innervation, primarily consisting of cholinergic fibers that originate from the vagus nerve (cranial nerve X) via the celiac plexus.^[9] These postganglionic fibers are identified through immunostaining for choline acetyltransferase and vesicular acetylcholine transporter, with cholinergic ganglion cells present within the renal nerve plexus in a subset of cases.^[9] Evidence for this innervation remains limited, as most studies emphasize sympathetic dominance, but retrograde tracing confirms a vagal brain-kidney axis involving projections from the dorsal motor nucleus of the vagus to the renal vasculature and pelvis.^[9] Functionally, these fibers may promote vasodilation in renal arteries and segmental branches through activation of muscarinic acetylcholine receptors, particularly mAChR3 expressed on endothelial cells, though direct physiological confirmation is ongoing.^[9] In contrast, sensory afferent fibers constitute a significant component of the renal plexus, comprising unmyelinated C-fibers and a smaller population of myelinated A-delta fibers that convey signals from the kidney to the central nervous system.^[10] These afferents are densest in the renal pelvis and papillae, with extensions to the cortex including glomeruli and tubules, enabling detection of mechanical and chemical stimuli.^[11] Projections ascend via dorsal root ganglia at spinal levels T10 to L1, entering the spinal cord through the dorsal horn (laminae I and III-V), and continue centrally to brainstem nuclei such as the nucleus tractus solitarius and rostral ventrolateral medulla, as well as the hypothalamic paraventricular nucleus.^[10]^[12] Afferent C-fibers primarily transmit nociceptive signals, eliciting visceral pain such as renal colic from obstruction, ischemia, or inflammation in the renal pelvis, while A-delta fibers contribute to sharper, localized sensations.^[10]^[13] Non-nociceptive roles include relaying information on osmoregulation and blood volume via mechanoreceptors and chemoreceptors, influencing systemic homeostasis through reflexes that modulate sympathetic outflow.^[11] Pain referral occurs to dermatomes T10-L1 in the anterior abdominal wall and flanks, mediated by pathways involving the least splanchnic nerve from the 12th thoracic paravertebral ganglion to the renal plexus.^[1]^[13]

Functions

Vascular regulation

The renal plexus provides sympathetic innervation to the renal vasculature, primarily through efferent fibers originating from the celiac and intermesenteric plexuses, which release norepinephrine to induce vasoconstriction.^[1] Sympathetic activation targets both afferent and efferent arterioles, causing constriction that reduces renal blood flow (RBF) and glomerular filtration rate (GFR), thereby conserving blood volume during stress responses.^[14] Under basal conditions, ongoing sympathetic tone from the renal plexus maintains RBF at approximately 20-25% of cardiac output, ensuring adequate perfusion for filtration while preventing excessive loss.^[14]^[15] Acute elevations in sympathetic activity, triggered by baroreceptor unloading or chemoreceptor stimulation during hypotension or hypoxia, further constrict renal vessels to redirect blood to vital organs, with the magnitude of response graded by the intensity of neural discharge.^[16] This neural control interacts with intrinsic renal autoregulation mechanisms, such as myogenic responses in vascular smooth muscle and tubuloglomerular feedback via the macula densa, where the plexus modulates tone without fully overriding these local safeguards that stabilize RBF across a wide range of perfusion pressures.^[2] Sympathetic fibers exhibit dense distribution around arcuate and interlobular arteries, as well as glomerular arterioles, enabling precise regulation of cortical and medullary blood distribution.^[14]

Renin-angiotensin system modulation

The renal plexus provides sympathetic innervation to the juxtaglomerular cells of the kidney, primarily through beta-1 adrenergic receptors, which stimulates renin secretion in response to reduced blood pressure or blood volume.^[1]^[17]^[18] Renin secreted by these cells cleaves circulating angiotensinogen to form angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme mainly in the pulmonary endothelium; angiotensin II promotes systemic vasoconstriction and stimulates aldosterone release from the adrenal cortex, resulting in renal sodium and water retention to restore blood volume and pressure.^[19]^[20] Chronic sympathetic overactivity mediated by the renal plexus enhances renin-angiotensin-aldosterone system (RAAS) activation, which sustains elevated blood pressure and contributes to renal injury through mechanisms such as glomerular hyperfiltration and fibrosis.^[21]^[22]^[23] Renal sympathetic nerve activity from the plexus correlates positively with plasma renin activity levels, where increased nerve firing thresholds directly elevate renin release and subsequent RAAS components.^[24]^[25]

Sensory transmission

The renal plexus contains afferent sensory fibers that transmit visceral sensations from the kidney, primarily originating from the renal pelvis and parenchyma. These unmyelinated C-fibers and thinly myelinated Aδ-fibers detect mechanical distension, ischemia, and inflammation, relaying signals to the central nervous system via the spinothalamic tract for processing of pain and other sensations.^[1]^[26] In conditions such as renal colic caused by ureteral obstruction, activation of these afferents leads to referred pain in the flank, lower abdomen, or costovertebral angle, often radiating in a dermatomal pattern due to convergence with somatic inputs at spinal levels T10-L1.^[1]^[27]^[28] Beyond nociception, low-threshold non-painful afferents in the renal plexus monitor renal interstitial osmolarity and volume changes, projecting to the hypothalamus to influence thirst mechanisms and antidiuretic hormone (ADH) release for fluid homeostasis.^[1]^[29]^[30] These C-fibers exhibit polymodal responsiveness, activating in response to noxious thermal stimuli or chemical irritants such as protons and capsaicin-like compounds.^[1]

Clinical significance

Role in hypertension

The renal plexus, primarily composed of sympathetic fibers, contributes to hypertension pathophysiology through elevated efferent sympathetic outflow that promotes renal sodium retention and impairs pressure natriuresis. This outflow stimulates alpha-1 adrenergic receptors on renal tubules, increasing sodium reabsorption and reducing urinary sodium excretion (natriuresis), which in turn expands extracellular fluid volume and sustains elevated arterial pressure.^[31]^[32] In essential hypertension, renal sympathetic nerve activity (RSNA) is elevated, contributing to overactivation of the renin-angiotensin-aldosterone system (RAAS) via increased renin release from juxtaglomerular cells and to endothelial dysfunction through oxidative stress and reduced nitric oxide bioavailability. This heightened RSNA correlates with disease severity and perpetuates a vicious cycle of vasoconstriction and vascular remodeling.^[33]^[34]^[35] Animal models of hypertension demonstrate the causal role of renal sympathetic activity, where renal denervation reduces systolic blood pressure by approximately 10-20 mmHg in spontaneously hypertensive rats and other rodent models by interrupting this pathway.^[36]^[37] Human evidence from microneurography studies, which measure muscle sympathetic nerve activity (MSNA) as a proxy for systemic sympathetic drive including RSNA, shows a strong positive correlation between elevated sympathetic burst rates and blood pressure levels in patients with essential hypertension.^[38]^[21]

Renal denervation procedures

Renal denervation procedures aim to disrupt the sympathetic innervation of the kidneys provided by the renal plexus to treat conditions such as resistant hypertension. The primary approach is catheter-based renal denervation (RDN), a minimally invasive endovascular technique performed via femoral artery access. In this method, a catheter is advanced to the renal arteries, where energy is delivered to ablate the perivascular nerves. Two main technologies are used: radiofrequency ablation, which employs electrodes to generate heat and target nerves up to 7 mm from the arterial lumen while sparing the endothelium, and ultrasound ablation, which uses a balloon-mounted transducer to emit focused energy waves, cooling the artery lumen to protect it during nerve disruption in the perivascular space.^[39]^[40] These procedures substantially reduce renal sympathetic nerve activity (RSNA), with preclinical animal models demonstrating 80-90% ablation of efferent sympathetic fibers, leading to decreased norepinephrine spillover and blood pressure lowering.^[41] Catheter-based RDN is indicated primarily for patients with resistant hypertension, defined as uncontrolled blood pressure despite adherence to at least three antihypertensive medications of different classes, including a diuretic. The procedure received CE Mark approval in Europe in 2010 for the Symplicity system, based on early open-label trials showing significant blood pressure reductions. In November 2023, the US Food and Drug Administration (FDA) approved two renal denervation systems—the Symplicity Spyral (Medtronic) and Paradise (Recor Medical)—for the treatment of hypertension in adults with uncontrolled blood pressure despite lifestyle and pharmacological interventions.^[40]^[42]^[39]^[40] Sham-controlled randomized trials, such as SPYRAL HTN-OFF MED and RADIANCE-HTN TRIO, have confirmed modest but consistent ambulatory systolic blood pressure reductions of 5-10 mm Hg at 3-6 months post-procedure compared to sham controls, with effects sustained up to 3 years or longer in follow-up data.^[40]^[42]^[39] As of 2025, renal denervation is included in the American College of Cardiology/American Heart Association (ACC/AHA) hypertension guidelines as an option for select patients with resistant hypertension.^[43] Historically, surgical renal denervation involved open procedures such as thoracolumbar sympathectomy, which interrupted renal sympathetic outflow during operations for severe hypertension in the mid-20th century; these were effective in reducing blood pressure by 20-30 mm Hg but carried high risks of morbidity, including orthostatic hypotension and sexual dysfunction, leading to their obsolescence with the advent of antihypertensive pharmacotherapy. Today, surgical approaches are rare and reserved for exceptional cases, supplanted by the safer, percutaneous catheter methods.^[40]^[44] Clinical outcomes of RDN show effectiveness in approximately 60-70% of patients, with sustained ambulatory systolic blood pressure reductions of 5-9 mm Hg observed up to 3 years in pivotal trials, though individual responses vary based on baseline sympathetic activity and procedural completeness. Risks are low overall, with major adverse events occurring in less than 1% of cases; potential complications include renal artery stenosis (0.2-2% incidence, typically within the first year and rarely requiring intervention) and partial reinnervation, which may occur over time but has not been shown to fully reverse blood pressure benefits in long-term follow-up.^[40]^[39]^[45] In renal transplantation, the procedure inherently results in complete denervation of the allograft due to surgical severance of the renal plexus, yet transplanted kidneys maintain normal function through intrinsic autoregulatory mechanisms, such as tubuloglomerular feedback, without reliance on extrinsic neural input.^[46]

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