Мақола

When kidneys and joints collide; bidirectional pathogenic crosstalk in CKD and osteoarthritis; from molecular mechanisms to clinical management

Kianoush SaberiDepartment of Anesthesiology, Medical Faculty, Imam Khomeini Hospital Complex, Tehran University of Medical Sciences, Tehran, IranSevara MukhammadievaTashkent State University of EconomicsSarvinoz IsirgapovaDepartment of Family Medicine No. 2, Clinical Pharmacology, Tashkent State Medical University, Tashkent, UzbekistanDavron KhozhimetovDepartment of Faculty and Hospital Surgery-2, Andijan State Medical Institute, Andijan, UzbekistanQaxramon MashrapovNamangan State Technical University, Namangan, UzbekistanMaxbuba NAZAROVADepartment of Biological Chemistry, Samarkand State Medical University, Samarkand, UzbekistanLola XamdamovaDepartment of Pediatric Dentistry, Bukhara State Medical Institute named after Abu Ali ibn Sino, Bukhara, UzbekistanDildora MengliyevaDepartment of Pediatric Dentistry, Bukhara State Medical Institute named after Abu Ali ibn Sino, Bukhara, UzbekistanSharifa RahmonovaDepartment of Stomatology and Otorhinolaryngology, Fergana Medical Institute of Public Health, Fergana, UzbekistanElham KebriyaeiClinical Research Development Unit, Valiasr Hospital, Fasa University of Medical Sciences, Fasa, Iran

2026en

ABI

Аннотация

Chronic kidney disease (CKD) and osteoarthritis frequently coexist, particularly in aging populations, imposing a significant burden on patients and healthcare systems. Emerging evidence reveals a complex, bidirectional pathogenic crosstalk between these conditions, extending beyond shared risk factors like aging and obesity. In CKD, the accumulation of uremic toxins, systemic inflammation driven by cytokines and disturbances in mineral bone disorder (CKD-MBD), characterized by dysregulated fibroblast growth factor-23 (FGF23), Klotho deficiency, hyperparathyroidism, and vascular calcification, actively contribute to accelerated articular cartilage degradation, synovitis, and subchondral bone sclerosis, thereby promoting osteoarthritis initiation and progression. Conversely, osteoarthritis-induced chronic pain, joint dysfunction, and reduced mobility lead to physical inactivity, sarcopenia, and metabolic dysregulation, potentially exacerbating CKD progression through strengthened inflammation, insulin resistance, and cardiovascular strain. This bidirectional relationship creates significant clinical challenges; since, standard osteoarthritis analgesics like non-steroidal anti-inflammatory drugs are nephrotoxic and contraindicated in chronic renal failure, since CKD-related complications complicate joint replacement surgery and rehabilitation. Effective management requires a paradigm shift towards integrated care. Treatment modalities include aggressive CKD-MBD control, cautious selection of joint-friendly analgesics, structured exercise programs tailored to renal and joint limitations, and early specialist collaboration. Identification of these intertwined molecular pathways is necessary for developing targeted therapies that simultaneously protect both renal and musculoskeletal health, eventually improving outcomes for this high-risk comorbid population.

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DOI: 10.34172/npj.12880

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