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Renal Inflammatory Response Mediated by Chronic Pain and Related Stress
Author(s) -
Duong Brittany B.,
Carder Misty L.,
Crosby Garrett S.,
Duric Vanja,
Babich Victor,
Di Sole Francesca
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.697.4
Subject(s) - medicine , kidney disease , chronic pain , inflammation , lipocalin , proinflammatory cytokine , renal function , kidney , immunology , physical therapy
Chronic pain is one the most distressing symptoms among patients with chronic kidney disease (CKD). The prevalence of chronic pain in CKD patients has been associated with development of depressive symptoms, while major depression episodes have been linked with a substantially increased risk of death. These evidences suggest that an effective treatment of chronic pain‐related stress and depression may reduce mortality in people with CKD. Moreover, chronic pain‐related stress can correlate to the development of mood disorders and disease of peripheral organs, such as kidney disease, via chronic systemic inflammation and elevation of proinflammatory cytokines. This study aims to determine whether an immune reaction is the mechanism that links depressive behavior induced by chronic pain and anomalies of kidney function. The neutrophil gelatinase‐associated lipocalin (NGAL) and IL‐18 are early diagnostic inflammatory biomarkers. They accumulate in the kidney in response to inflammation, kidney injury and decreased kidney function. Protein levels of NGAL and IL18 were analyzed by immunocytochemistry in animals exposed to chronic pain that have developed depressive‐like behavioral phenotype. NGAL and IL18 protein levels were significantly increased in rat models of neuropathic (spared nerve injury) and inflammatory (injections of complete Freund's adjuvant) pain when compared with their controls; a prevalent increase in NGAL and IL18 protein levels was measured in the inflammatory pain model (~40% increase in both glomeruli and tubules, quantified using novel MATLAB algorithm). These observations suggest that chronic pain and related stress effects induce renal inflammation and possibly a reduction in kidney function. In summary, this study might support a mechanistic understanding of a bidirectional pathway between chronic pain related‐stress and kidney dysfunction.