Complement in Non-Antibody-Mediated Kidney Diseases

Angeletti, Andrea; Reyes-Bahamonde, Joselyn; Cravedi, Paolo

doi:10.3389/fmed.2017.00099

Cited by 13 publications

(11 citation statements)

References 110 publications

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“…The complement system is part of the innate immune response with the main function of protecting the host from foreign pathogens [17][18][19]. The complement cascade is activated by the lectin pathway, the classical pathway and the alternative pathway, all of them converging on an enzymatic multimeric protein complex, the C3 convertase [18].…”

Section: Complement Systemmentioning

confidence: 99%

Immunological Effects of a Single Hemodialysis Treatment

et al. 2020

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Immune disorders, involving both innate and adaptive response, are common in patients with end-stage renal disease under chronic hemodialysis. Endogenous and exogenous factors, such as uremic toxins and the extracorporeal treatment itself, alter the immune balance, leading to chronic inflammation and higher risk of cardiovascular events. Several studies have previously described the immune effects of chronic hemodialysis and the possibility to modulate inflammation through more biocompatible dialyzers and innovative techniques. On the other hand, very limited data are available on the possible immunological effects of a single hemodialysis treatment. In spite of the lacking information about the immunological reactivity related to a single session, there is evidence to indicate that mediators of innate and adaptive response, above all complement cascade and T cells, are implicated in immune system modulation during hemodialysis treatment. Expanding our understanding of these modulations represents a necessary basis to develop pro-tolerogenic strategies in specific conditions, like hemodialysis in septic patients or the last session prior to kidney transplant in candidates for receiving a graft.

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Section: Complement Systemmentioning

confidence: 99%

Immunological Effects of a Single Hemodialysis Treatment

et al. 2020

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“…Increasing evidence has been accumulated showing that complement activation is implicated in the pathogenesis of different non-antibody-mediated glomerular diseases and in the general progression of renal disease, regardless of the initial insult (Angeletti et al, 2017). Complement proteins are a major constituent of the urine of proteinuric patients (Proteinuria is a strong predictor of progression in CKD).…”

Section: Introductionmentioning

confidence: 99%

Estimation of Complement Components (C3 and C4) and hs-CRP Level in Kidney Failure Patients

Elia

Mustafa

2019

Polytechnic j.

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Several kidney diseases associated with complement activation. Complement activation occurs in progressive chronic kidney disease and may contribute to the chronic inflammation that is characteristically found in the kidney. This study was aimed to detect the level of complement system in kidney failure patients. This study was included (30) patients with renal failure and (15) healthy donors as control group. Serum samples separated from the whole blood of patients and healthy individuals. C3, C4, and high sensitive C- reactive protein (hsCRP) levels were estimated for all samples. The results were analyzed according to patients who were dialysis, non-dialysis, with diabetes, without diabetes, with high blood pressure, and without high blood pressure. The results showed that there was a significant increase (P < 0.05) in C3 level for patients with renal failure (154.12 mg/dl) compared to control group (126.08 mg/dl) while C4 level for renal failure patients (35.38 mg/dl) showed no significant change compared to control group (36.26 mg/dl). However, C3 level of patients under dialysis (152.15 mg/dl), not dialysis (162.01 mg/dl), with diabetic (155.80 mg/dl), and without diabetic (153 mg/dl) recorded significant elevation compared with control group (126.08 mg/dl) but C4 level did not show any significant change for all groups. C3 and C4 concentrations did not record significant alteration (P < 0.05) in patient with hypertension, nonhypertension, and control group. Moreover, seropositivity of CRP for patients with renal failure was ranged from 33.33% to 60% in all patients groups included in this study. hsCRP concentration significantly elevated (P < 0.05) in under dialysis (1.787 mg/L), nondialysis (1.583 mg/L), with diabetic (2.766 mg/L), nondiabetic (1.066 mg/L), with hypertension (1.84 mg/L), and nonhypertension (1.26 mg/L) when compared with control group (0.667 mg/L). The present findings suggest that the increased serum levels of C3, C4, and hs-CRP reflect the of kidney injury. Hence, this reflects the complement system as an important mediator of kidney injury and the role of anti-complement therapy in nephropathy will expand in the future.

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“…In accordance, studies in rodent knockout showed that the absence of C3aR and C5aR on renal tubular epithelial cells or circulating leukocytes attenuated renal IRI. Treatment in vivo using antagonist for C3aR and C5aR and for factor B could improve graft survival, reducing the decrease in renal injury, tubular apoptosis, and inflammation (216,220,221).…”

Section: Cell-specific Effects Of Complement In Aki-to-ckd Transitionmentioning

confidence: 99%

Inflammaging and Complement System: A Link Between Acute Kidney Injury and Chronic Graft Damage

et al. 2020

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The aberrant activation of complement system in several kidney diseases suggests that this pillar of innate immunity has a critical role in the pathophysiology of renal damage of different etiologies. A growing body of experimental evidence indicates that complement activation contributes to the pathogenesis of acute kidney injury (AKI) such as delayed graft function (DGF) in transplant patients. AKI is characterized by the rapid loss of the kidney’s excretory function and is a complex syndrome currently lacking a specific medical treatment to arrest or attenuate progression in chronic kidney disease (CKD). Recent evidence suggests that independently from the initial trigger (i.e., sepsis or ischemia/reperfusions injury), an episode of AKI is strongly associated with an increased risk of subsequent CKD. The AKI-to-CKD transition may involve a wide range of mechanisms including scar-forming myofibroblasts generated from different sources, microvascular rarefaction, mitochondrial dysfunction, or cell cycle arrest by the involvement of epigenetic, gene, and protein alterations leading to common final signaling pathways [i.e., transforming growth factor beta (TGF-β), p16ink4a, Wnt/β-catenin pathway] involved in renal aging. Research in recent years has revealed that several stressors or complications such as rejection after renal transplantation can lead to accelerated renal aging with detrimental effects with the establishment of chronic proinflammatory cellular phenotypes within the kidney. Despite a greater understanding of these mechanisms, the role of complement system in the context of the AKI-to-CKD transition and renal inflammaging is still poorly explored. The purpose of this review is to summarize recent findings describing the role of complement in AKI-to-CKD transition. We will also address how and when complement inhibitors might be used to prevent AKI and CKD progression, therefore improving graft function.

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Complement in Non-Antibody-Mediated Kidney Diseases

Cited by 13 publications

References 110 publications

Immunological Effects of a Single Hemodialysis Treatment

Immunological Effects of a Single Hemodialysis Treatment

Estimation of Complement Components (C3 and C4) and hs-CRP Level in Kidney Failure Patients

Inflammaging and Complement System: A Link Between Acute Kidney Injury and Chronic Graft Damage

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