Is IL-33 useful to detect early stage of renal failure?

Caner, Sedat; Usluoğulları, Celil Alper; Balkan, Fevzi; Büyükcam, Fatih; Kaya, Cafer; Sacikara, Muhammed; Koca, Cemile; Ersoy, Reyhan; Çakır, Bekir

doi:10.3109/0886022x.2013.832313

Cited by 14 publications

(16 citation statements)

References 10 publications

(12 reference statements)

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“…However, there was no difference when diabetic patients with or without nephropathy were compared. The results of this study suggest that IL-33 cannot be used as a marker of renal injury [48]. IL-6 is a proinflammatory cytokine and an important mediator of cell proliferation, endothelial cell permeability and increase in matrix production [55].…”

Section: Proinflammatory Cytokines and Dnmentioning

confidence: 84%

Cytokines and T Helper Cells in Diabetic Nephropathy Pathogenesis

Araújo¹,

Silva²,

Silva³

et al. 2016

JDM

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Diabetic Nephropathy (DN) is considered the main cause of end stage kidney disease around the world. However, its pathogenesis is not completely established. More than just a direct consequence of chronic glycemic changes, recent studies had suggested Diabetic Nephropathy could be considered an inflammatory disease. It has been shown that concentrations of pro-inflammatory cytokines, as IL-1, IL-6, IL-18, IL-33, IFN-γ and TNF-α actively participate in development and progression of DN, and thus, are involved in pathogenesis. Besides, changes in acquired immune response, especially the presence of cellular immune response profiles of pro-inflammatory and effector nature, mainly Th1 and Th17, as the imbalance between interaction of cytokines and T regulatory cells, foment the onset and progression of DN. Here we summarize the main evidences that support the critical role of the immune system in this condition. These new conceptual advances in DN understanding are essential for development of new the rapeutical strategies and prognostic factors, which could be protagonists or adjuvants to the current ones, leading ultimately to a better clinical management of DN patients.

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Section: Proinflammatory Cytokines and Dnmentioning

confidence: 84%

Cytokines and T Helper Cells in Diabetic Nephropathy Pathogenesis

Araújo¹,

Silva²,

Silva³

et al. 2016

JDM

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“…IL-33 serum levels of CKD patients were not significantly changed in the three groups but serum levels of sST2 strongly correlated with severity of the disease [58]. Another report by Caner et al demonstrated that IL-33 serum level was not better in early recognition of diabetic nephropathy [59]. The increase in IL-33 serum levels in diabetic nephropathy was not associated with kidney injury, whereas the increase might be a result of diabetes [59].…”

Section: Il-33 In Chronic Kidney Injurymentioning

confidence: 99%

“…Another report by Caner et al demonstrated that IL-33 serum level was not better in early recognition of diabetic nephropathy [59]. The increase in IL-33 serum levels in diabetic nephropathy was not associated with kidney injury, whereas the increase might be a result of diabetes [59]. Musolino et al reported that reduced IL-33 serum levels in multiple myeloma (MM) patients were associated with a more advanced stage of disease [60].…”

Section: Il-33 In Chronic Kidney Injurymentioning

confidence: 99%

“…Inflammatory responses are wildly triggered during DN progression, hence, inflammatory cytokines are profoundly involved in disease progression and severity; IL-33 has emerged as a candidate that is closely involved in the pathogenesis of DN [62]. A recent clinical study by Caner and colleagues investigated the association between IL-33 and DN by analyzing the serum levels of IL-33 from a healthy group, a diabetes mellitus (DM) group without any known renal diseases, and a DM group with microalbuminuria (MA) [59]. The results of Caner’s study demonstrated that IL-33 levels in the DM and DM with MA groups were greater than the healthy group.…”

Section: Il-33 In Chronic Kidney Injurymentioning

confidence: 99%

“…The results of Caner’s study demonstrated that IL-33 levels in the DM and DM with MA groups were greater than the healthy group. No significant difference on serum levels of IL-33 was observed between the DM group and the DM with MA group [59]. Therefore, diabetes per se upregulates the serum level of IL-33, but it is not suitable to be used for early diagnosis of DN.…”

Section: Il-33 In Chronic Kidney Injurymentioning

confidence: 99%

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Emerging Roles of IL-33/ST2 Axis in Renal Diseases

Chen

Yang

2017

IJMS

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Renal diseases, including acute kidney injury (AKI) and chronic kidney disease (CKD), have a great impact on health care systems worldwide. Similar to cardiovascular diseases, renal diseases are inflammatory diseases involving a variety of cytokines. Primary causes of renal injury include ischemia, uremic toxins, bacteremia, or nephrotoxicity. Inflammation represents an important component following kidney injury. Interleukin (IL)-33 is a member of the IL-1 cytokine family, which is widely expressed in epithelial barrier tissues and endothelial cells, and mediates both tissue inflammation and repair responses. IL-33 is released as a nuclear alarmin in response to tissue damage and triggers innate and adaptive immune responses by binding to its receptor, suppression of tumorigenicity 2 (ST2). Recent evidence from clinical and experimental animal studies indicates that the IL-33/ST2 axis is involved in the pathogenesis of CKD, renal graft injury, systemic lupus nephritis, and AKI. In this review, we discuss the pathological and tissue reparative roles of the IL-33/ST2 pathway in different types of renal diseases.

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Review of potential biomarkers of inflammation and kidney injury in diabetic kidney disease

Khanijou

Zafari

Coughlan

et al. 2022

Diabetes Metabolism Res

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Diabetic kidney disease is expected to increase rapidly over the coming decades with rising prevalence of diabetes worldwide. Current measures of kidney function based on albuminuria and estimated glomerular filtration rate do not accurately stratify and predict individuals at risk of declining kidney function in diabetes. As a result, recent attention has turned towards identifying and assessing the utility of biomarkers in diabetic kidney disease. This review explores the current literature on biomarkers of inflammation and kidney injury focussing on studies of single or multiple biomarkers between January 2014 and February 2020. Multiple serum and urine biomarkers of inflammation and kidney injury have demonstrated significant association with the development and progression of diabetic kidney disease. Of the inflammatory biomarkers, tumour necrosis factor receptor-1 and -2 were frequently studied and appear to hold most promise as markers of diabetic kidney disease.With regards to kidney injury biomarkers, studies have largely targeted markers of tubular injury of which kidney injury molecule-1, beta-2-microglobulin and neutrophil gelatinase-associated lipocalin emerged as potential candidates. Finally, the use of a small panel of selective biomarkers appears to perform just as well as a panel of multiple biomarkers for predicting kidney function decline.

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Is IL-33 useful to detect early stage of renal failure?

Cited by 14 publications

References 10 publications

Cytokines and T Helper Cells in Diabetic Nephropathy Pathogenesis

Cytokines and T Helper Cells in Diabetic Nephropathy Pathogenesis

Emerging Roles of IL-33/ST2 Axis in Renal Diseases

Review of potential biomarkers of inflammation and kidney injury in diabetic kidney disease

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