Renal nerves and their role in physiology and disease have been a topic of increasing interest in the past few decades. Renal inflammation contributes to many cardiorenal disease conditions, including hypertension, chronic kidney disease, and polycystic kidney disease. Much is known about the role of renal sympathetic nerves in physiology - they contribute to the regulation of sodium reabsorption, renin release, and renal vascular resistance. In contrast, far less is known about afferent, or "sensory," renal nerves, which convey signals from the kidney to the brain. While much remains unknown about these nerves in the context of normal physiology, even less is known about their contribution to disease states. Furthermore, it has become apparent that the crosstalk between renal nerves and the immune system may augment or modulate disease. Research from other fields, especially pain research, has provided critical insight into neuroimmune crosstalk. Sympathetic renal nerve activity may increase immune cell recruitment, but far less work has been done investigating the interplay between afferent renal nerves and the immune system. Evidence from other fields suggests that inflammation may augment afferent renal nerve activity. Furthermore, these nerves may exacerbate renal inflammation through the release of afferent-specific neurotransmitters.
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http://dx.doi.org/10.1016/j.autneu.2023.103133 | DOI Listing |
Medicina (Kaunas)
January 2025
Department of Anesthesiology and Pain Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
: Kidney transplantation (KT) is an important treatment modality for renal failure. However, moderate-to-severe pain often occurs in KT recipients. Multimodal analgesia using combined analgesic measures has been recommended to enhance postoperative recovery.
View Article and Find Full Text PDFBiomedicines
January 2025
Second Department of Internal Medicine, Division of Nephrology, Kansai Medical University, Hirakata 573-1010, Japan.
: Charcot-Marie-Tooth (CMT) disease is an inherited peripheral neuropathy primarily involving motor and sensory neurons. Mutations in INF2, an actin assembly factor, cause two diseases: peripheral neuropathy CMT-DIE (MIM614455) and/or focal segmental glomerulosclerosis (FSGS). These two phenotypes arise from the progressive degeneration affecting podocytes and Schwann cells.
View Article and Find Full Text PDFJ Arthroplasty
January 2025
Department of Orthopaedic Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-Ku, Sendai, Miyagi, 980-8574, Japan.
Background: Osteonecrosis of the femoral head (ONFH) and osteoarthritis (OA) are two common diagnoses for patients undergoing total hip arthroplasty (THA). The early surgical complications in THA for ONFH compared to OA are inconsistently reported. Therefore, this study aimed to evaluate whether THA for ONFH was associated with early postoperative complications in comparison to THA for OA using a large database of Japanese patients.
View Article and Find Full Text PDFTurk Neurosurg
March 2024
SBÜ Gaziosmanpaşa Eğitim ve Araştırma Hastanesi.
Erdheim-Chester Disease is a rare systemic xanthogranulomatous infiltrating disease, characterized by lipid-laden histiocytes accumulating in various organs and almost always in bones. Etiology of the disease is still unknown. It may involve various organs and systems, such as musculoskeletal, cardiac, pulmonary, renal, gastrointestinal and central nervous system (CNS) as well as the skin.
View Article and Find Full Text PDFHypertension
January 2025
Department of Environmental Health, Life Science and Human Technology, Nara Women's University, Japan.
Background: Exposure to cold environments is linked to cold-induced hypertension due to activated sympathetic nerve activity (SNA) and arterial baroreceptor reflex dysfunction. However, direct measurement of SNA during cold-induced hypertension and changes in baroreflex control of SNA remain unexplored.
Methods: Chronically instrumented rats were exposed to cold temperatures (10 °C) over 4 days after a control period (24 °C), and renal and lumbar sympathetic nerve activities were simultaneously measured during cold-induced hypertension.
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