Life 2026, 16(8), 1354; https://doi.org/10.3390/life16081354 (registering DOI) - 18 Aug 2026
Abstract
Chronic pain is one of the most common and disabling complications of chronic kidney disease (CKD), yet it is almost exclusively viewed as a consequence of declining kidney function. This perspective overlooks the possibility that chronic pain itself may influence the biological processes
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Chronic pain is one of the most common and disabling complications of chronic kidney disease (CKD), yet it is almost exclusively viewed as a consequence of declining kidney function. This perspective overlooks the possibility that chronic pain itself may influence the biological processes driving CKD progression. Chronic pain is being recognized as a systemic disorder characterized by sustained neuroimmune activation, inflammation, oxidative stress, endothelial dysfunction, autonomic imbalance, mitochondrial impairment and maladaptive behavioral changes. These same mechanisms are also central to progressive kidney injury, raising the possibility that persistent pain may reinforce established pathogenic pathways rather than simply accompany them. We propose a conceptual framework in which chronic pain functions as a disease modifier capable of amplifying the biological and clinical processes that contribute to CKD progression. Although this hypothesis does not imply that chronic pain directly causes CKD or that pain management is inherently renoprotective, it provides a biologically plausible rationale for investigating whether pain contributes to disease progression beyond serving as a marker of disease severity. Exploring this possibility may broaden current concepts of CKD progression and identify new directions for mechanistic, translational and clinical research.
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(This article belongs to the Special Issue CKD and Glomerular Diseases)
