Spondyloarthritis Patients Suffer Increased Risk of Renal Complications Compared With General Population: A Retrospective Observational Study

Xiao, Min; Lv, Qing; Tu, Liudan; Yang, Mingcan; Liao, Zetao; Jiang, Yutong; Zheng, Xuqi; Li, Xiaomin; Wei, Qiujing; Cao, Shuangyan; J, Gu

doi:10.3389/fphar.2019.01073

Cited by 6 publications

(2 citation statements)

References 33 publications

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“…Additional evidence about the role of the Th17/IL-17 axis on Kidney diseases comes from the observation of the increased risk of CKD associated with renal inflammation in human diseases that occur with the hyperactivation of the Th17/IL-17 axis, like psoriasis (210)(211)(212), rheumatoid arthritis (213,214), and ankylosing spondylitis (215)(216)(217). In two studies (in the United Kingdom and Taiwan), psoriasis was associated with an increased risk of chronic kidney disease independent of traditional risk factors (211,212).…”

Section: The Association Between Th17/il-17 Axis Hyperactivity and Several Kidney Diseases (Other Than Lupus Nephritis)mentioning

confidence: 99%

The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis

Paquissi

Abensur

2021

Front. Med.

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Systemic lupus erythematosus (SLE) is a disease characterized by dysregulation and hyperreactivity of the immune response at various levels, including hyperactivation of effector cell subtypes, autoantibodies production, immune complex formation, and deposition in tissues. The consequences of hyperreactivity to the self are systemic and local inflammation and tissue damage in multiple organs. Lupus nephritis (LN) is one of the most worrying manifestations of SLE, and most patients have this involvement at some point in the course of the disease. Among the effector cells involved, the Th17, a subtype of T helper cells (CD4+), has shown significant hyperactivation and participates in kidney damage and many other organs. Th17 cells have IL-17A and IL-17F as main cytokines with receptors expressed in most renal cells, being involved in the activation of many proinflammatory and profibrotic pathways. The Th17/IL-17 axis promotes and maintains repetitive tissue damage and maladaptive repair; leading to fibrosis, loss of organ architecture and function. In the podocytes, the Th17/IL-17 axis effects include changes of the cytoskeleton with increased motility, decreased expression of health proteins, increased oxidative stress, and activation of the inflammasome and caspases resulting in podocytes apoptosis. In renal tubular epithelial cells, the Th17/IL-17 axis promotes the activation of profibrotic pathways such as increased TGF-β expression and epithelial-mesenchymal transition (EMT) with consequent increase of extracellular matrix proteins. In addition, the IL-17 promotes a proinflammatory environment by stimulating the synthesis of inflammatory cytokines by intrinsic renal cells and immune cells, and the synthesis of growth factors and chemokines, which together result in granulopoiesis/myelopoiesis, and further recruitment of immune cells to the kidney. The purpose of this work is to present the prognostic and immunopathologic role of the Th17/IL-17 axis in Kidney diseases, with a special focus on LN, including its exploration as a potential immunotherapeutic target in this complication.

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Section: The Association Between Th17/il-17 Axis Hyperactivity and Several Kidney Diseases (Other Than Lupus Nephritis)mentioning

confidence: 99%

The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis

Paquissi

Abensur

2021

Front. Med.

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“…Inflammatory effects of IndSO4 have been investigated in chronic kidney disease, where it disrupts the intestinal barrier and contributes to inflammation via activation of the nuclear factor kappa B signalling pathway 22 . Of note, decreased kidney function is a potential complication of GI and MSK CID 23,24 . Two other Trp derivatives displayed notable trends relative to the healthy population tested: serotonin and IPA.…”

Section: Mainmentioning

confidence: 99%

Tryptophan wasting and disease activity as a systems phenomenon in inflammation – an analysis across 13 chronic inflammatory diseases

Harris,

Szymczak,

Schuchardt

et al. 2023

Preprint

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Chronic inflammatory diseases (CID) are systems disorders affecting various organs including the intestine, joint and skin. The essential amino acid tryptophan (Trp) is not only used for protein synthesis but can also be catabolized to various bioactive derivatives that are important for cellular energy metabolism and immune regulation. Increased Trp catabolism via the kynurenine pathway is seen across individual CID entities1–5. Here, we assessed the levels of Trp and tryptophan derivatives across 13 CID to investigate the extent and nature of Trp wasting as a systems phenomenon in CID. We found reduced serum Trp levels across the majority of CID and a prevailing negative relationship between Trp and systemic inflammatory marker C-reactive protein (CRP). Increases in the kynurenine-to-Trp ratio (Kyn:Trp) indicate that the kynurenine pathway is a major route for CID-related Trp wasting. However, the extent of Trp depletion and its relationship with disease activity varies by disease, indicating potential differences in Trp metabolism. In addition, we find that amino acid catabolism in chronic inflammation is specific to tryptophan wasting, whereas other proteinogenic amino acids are not affected. Hence, our results suggest that increased Trp catabolism is a common metabolic occurrence in CID that may directly affect systemic immunity.Grant supportThis work was supported by the DFG Cluster of Excellence 1261 “Precision medicine in chronic inflammation” (KA, SSchr, PR, BH, SWa), the BMBF (e:Med Juniorverbund “Try-IBD” 01ZX1915A and 01ZX2215, the e:Med Network iTREAT 01ZX2202A, and GUIDE-IBD 031L0188A), DFG RU5042 (PR, KA), and Innovative Medicines Initiative 2 Joint Undertakings (“Taxonomy, Treatments, Targets and Remission”, No. 831434, “ImmUniverse”, grant agreement No. 853995, “BIOMAP”, grant agreement No. 821511).

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