Inflammation in Nonimmune-Mediated Chronic Kidney Disease

Fanelli, Camilla; Noreddin, Ayman M.; Nunes, Ane Cláudia Fernandes

doi:10.5772/intechopen.70611

Cited by 7 publications

(8 citation statements)

References 55 publications

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“…153 The molecular mechanisms of inflammation associated with CKD are beyond the scope of this review; however, a summary of both innate and adaptive inflammatory processes in CKD has recently been published. 154 Elements of the adaptive response to acidosis, particularly upregulation of angiotensin II, have been associated with kidney infiltration by leukocytes. 121,122,155 In vitro and in vivo evidence suggests that angiotensin II promotes cell proliferation and fibroblast activation, worsening abnormal accumulation of extracellular matrix in the damaged kidney and contributing to development of kidney fibrosis and inflammation.…”

Section: Cellular Damage To the Kidney Caused By Chronic Metabolic Acmentioning

confidence: 99%

Mechanisms of Metabolic Acidosis–Induced Kidney Injury in Chronic Kidney Disease

Wesson

Buysse

Bushinsky

2020

JASN

133

108

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Retrospective analyses and single-center prospective studies identify chronic metabolic acidosis as an independent and modifiable risk factor for progression of CKD. In patients with CKD, untreated chronic metabolic acidosis often leads to an accelerated reduction in GFR. Mechanisms responsible for this reduction include adaptive responses that increase acid excretion but lead to a decline in kidney function. Metabolic acidosis in CKD stimulates production of intrakidney paracrine hormones including angiotensin II, aldosterone, and endothelin-1 (ET-1) that mediate the immediate benefit of increased kidney acid excretion, but their chronic upregulation promotes inflammation and fibrosis. Chronic metabolic acidosis also stimulates ammoniagenesis that increases acid excretion but also leads to ammonia-induced complement activation and deposition of C3 and C5b-9 that can cause tubule-interstitial damage, further worsening disease progression. These effects, along with acid accumulation in kidney tissue, combine to accelerate progression of kidney disease. Treatment of chronic metabolic acidosis attenuates these adaptive responses; reduces levels of angiotensin II, aldosterone, and ET-1; reduces ammoniagenesis; and diminishes inflammation and fibrosis that may lead to slowing of CKD progression.Published online ahead of print. Publication date available at www.jasn.org.

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Section: Cellular Damage To the Kidney Caused By Chronic Metabolic Acmentioning

confidence: 99%

Mechanisms of Metabolic Acidosis–Induced Kidney Injury in Chronic Kidney Disease

Wesson

Buysse

Bushinsky

2020

JASN

133

108

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“…The persistent low-grade inflammatory status that characterizes CKD plays a key role in the pathophysiology of the disease. Inflammation starts early in the onset of renal diseases [ 13 , 14 ] and worsens with disease progression [ 15 ], being particularly marked in hemodialysis patients [ 16 ]. Interestingly, inflammation can be identified either as a trigger or a consequence of CKD.…”

Section: Inflammation As An Essential Component Of Ckdmentioning

confidence: 99%

The Signaling Pathway of TNF Receptors: Linking Animal Models of Renal Disease to Human CKD

Lousa

Reis

Santos‐Silva

et al. 2022

IJMS

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Chronic kidney disease (CKD) has been recognized as a global public health problem. Despite the current advances in medicine, CKD-associated morbidity and mortality remain unacceptably high. Several studies have highlighted the contribution of inflammation and inflammatory mediators to the development and/or progression of CKD, such as tumor necrosis factor (TNF)-related biomarkers. The inflammation pathway driven by TNF-α, through TNF receptors 1 (TNFR1) and 2 (TNFR2), involves important mediators in the pathogenesis of CKD. Circulating levels of TNFRs were associated with changes in other biomarkers of kidney function and injury, and were described as predictors of disease progression, cardiovascular morbidity, and mortality in several cohorts of patients. Experimental studies describe the possible downstream signaling pathways induced upon TNFR activation and the resulting biological responses. This review will focus on the available data on TNFR1 and TNFR2, and illustrates their contributions to the pathophysiology of kidney diseases, their cellular and molecular roles, as well as their potential as CKD biomarkers. The emerging evidence shows that TNF receptors could act as biomarkers of renal damage and as mediators of the disease. Furthermore, it has been suggested that these biomarkers could significantly improve the discrimination of clinical CKD prognostic models.

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“…CKD pathogenesis’s leading and fundamental cause is linked to oxidative stress [ 2 ]. Fibrosis, tubulointerstitial inflammation, and glomerulosclerosis are structural changes seen in CKD patients’ glomeruli and tubular cells [ 3 ] The progression of CKD may advance to renal failure, and in that case, dialysis or kidney transplantation might be urgent and required [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanistic Pathways Targeted by Natural Antioxidants in the Prevention and Treatment of Chronic Kidney Disease

2021

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Chronic kidney disease (CKD) is the progressive loss of renal function and the leading cause of end-stage renal disease (ESRD). Despite optimal therapy, many patients progress to ESRD and require dialysis or transplantation. The pathogenesis of CKD involves inflammation, kidney fibrosis, and blunted renal cellular antioxidant capacity. In this review, we have focused on in vitro and in vivo experimental and clinical studies undertaken to investigate the mechanistic pathways by which these compounds exert their effects against the progression of CKD, particularly diabetic nephropathy and kidney fibrosis. The accumulated and collected data from preclinical and clinical studies revealed that these plants/bioactive compounds could activate autophagy, increase mitochondrial bioenergetics and prevent mitochondrial dysfunction, act as modulators of signaling pathways involved in inflammation, oxidative stress, and renal fibrosis. The main pathways targeted by these compounds include the canonical nuclear factor kappa B (NF-κB), canonical transforming growth factor-beta (TGF-β), autophagy, and Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid factor 2-related factor 2 (Nrf2)/antioxidant response element (ARE). This review presented an updated overview of the potential benefits of these antioxidants and new strategies to treat or reduce CKD progression, although the limitations related to the traditional formulation, lack of standardization, side effects, and safety.

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Inflammation in Nonimmune-Mediated Chronic Kidney Disease

Cited by 7 publications

References 55 publications

Mechanisms of Metabolic Acidosis–Induced Kidney Injury in Chronic Kidney Disease

Mechanisms of Metabolic Acidosis–Induced Kidney Injury in Chronic Kidney Disease

The Signaling Pathway of TNF Receptors: Linking Animal Models of Renal Disease to Human CKD

Molecular Mechanistic Pathways Targeted by Natural Antioxidants in the Prevention and Treatment of Chronic Kidney Disease

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