Authors: Yang S et al.
Anesthesiology, November 2025. DOI: 10.1097/ALN.0000000000005829
This large-scale cohort analysis used UK Biobank data from over 20,000 adults with diabetes to investigate how chronic pain patterns and analgesic use affect the risk of developing chronic kidney disease (CKD). Over a median follow-up of 13.2 years, participants with chronic pain had an 18% higher adjusted risk of incident CKD compared to those without chronic pain. The risk rose progressively with the number of pain sites, particularly when pain involved the neck/shoulder, back, hip, knee, or abdominal regions.
Interestingly, opioid use was independently linked to higher CKD risk (adjusted HR 1.22), while ibuprofen and paracetamol were not. Through metabolomic and proteomic analyses, the authors identified several biological signatures associated with pain-related CKD risk, including elevated chromogranin-A, increased glycoprotein acetyls, and a lower omega-3 to total fatty acids ratio. Network mapping suggested key roles for tumor necrosis factor (TNF) and epidermal growth factor receptor (EGFR) signaling in mediating these effects.
The authors conclude that multisite chronic pain and opioid use may accelerate CKD development in diabetic populations, mediated by inflammation and metabolic dysregulation. These results reinforce the need for integrated pain and renal management strategies in diabetic patients.
What You Should Know:
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Chronic pain—especially multisite pain—is an independent predictor of CKD among people with diabetes.
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Opioid therapy, but not non-opioid analgesics, is linked to increased renal risk.
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Metabolomic and proteomic data suggest inflammatory and metabolic pathways (TNF, EGFR) may connect pain physiology to renal injury.
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Clinicians should weigh kidney risk when selecting long-term pain management strategies for diabetic patients.
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