The Role of Oxidative Stress and Inflammation in Acute Oxalate Nephropathy Associated With Ethylene Glycol Intoxication

Wilson, Gregory J.; Gois, Pedro Henrique França; Zhang, Alice; Wang, Xiangju; Law, Betty Yuen‐Kwan; Kassianos, Andrew J.; Healy, Helen

doi:10.1016/j.ekir.2018.05.005

Cited by 7 publications

(5 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Consistently, tubular epithelial cell damage induced by tubular and interstitial calcium oxalate deposition, tubular atrophy and interstitial fibrosis have been described in humans [14]. In addition, oxalate alone has been recently associated with renal and systemic inflammation [15,120]. Its deposition in renal parenchyma resulted in activation of the innate immune system, driven by release of interleukin-1β via NLRP3 inflammasome (nucleotide-binding domain, leucine-rich repeat inflammasome 3) activation in dendritic cells and leading to progressive renal function decline in both acute and chronic animal models of tissue oxalate deposition [15,106,121].…”

Section: Chronic Kidney Diseasementioning

confidence: 69%

Dietary Oxalate Intake and Kidney Outcomes

et al. 2020

View full text Add to dashboard Cite

Oxalate is both a plant-derived molecule and a terminal toxic metabolite with no known physiological function in humans. It is predominantly eliminated by the kidneys through glomerular filtration and tubular secretion. Regardless of the cause, the increased load of dietary oxalate presented to the kidneys has been linked to different kidney-related conditions and injuries, including calcium oxalate nephrolithiasis, acute and chronic kidney disease. In this paper, we review the current literature on the association between dietary oxalate intake and kidney outcomes.

show abstract

Section: Chronic Kidney Diseasementioning

confidence: 69%

Dietary Oxalate Intake and Kidney Outcomes

et al. 2020

View full text Add to dashboard Cite

show abstract

“…The subsequent dimerization and maturation of caspase‐1 leads to the maturation and secretion of pro‐inflammatory cytokines (interleukin [IL]‐1β and IL‐18) . Inflammasomes are widely implicated in a variety of renal injuries, including acute and chronic kidney disease, oxalate nephropathy and uric acid crystal nephropathy . Based on our findings, we propose a functional role for increased DC and macrophages identified in our case study, which sense tubular oxidative stress via the inflammasome.…”

Section: Discussionmentioning

confidence: 52%

Role of inflammation and inflammasome activation in human bile cast nephropathy

et al. 2020

Self Cite

View full text Add to dashboard Cite

Bile cast nephropathy (BCN) is an underdiagnosed cause of acute kidney injury (AKI).The precise pathogenesis of bilirubin tubular toxicity remains unknown. The aim of this study is to explore the cellular and molecular pathophysiology of human BCN.Paraffin-embedded sections of renal biopsy tissue from a BCN patient were stained by immunohistochemistry (IHC) for oxidative stress (4-hydroxynonenal), immune cell subpopulations, including dendritic cells (CD1c), macrophages (CD68) and T cells (CD3), and inflammasome activation by staining for active-caspase-1 and the inflammasome adaptor protein, ASC (apoptosis-associated speck-like protein containing a caspase activation and recruitment domain). Quantitative analyses of IHC staining were com-

show abstract

“…The inflammasomes are a family of cytosolic signalling complexes with a central role in the activation of innate immune responses via the maturation and secretion of pro-inflammatory cytokines (interleukin (IL)-1β and IL-18) [18]. In particular, the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome, an extensively characterized inflammasome family member, is widely implicated in a variety of renal injuries, including acute and chronic kidney disease (CKD) [19,20,21]; oxalate and uric acid crystal nephropathy [22,23]; and diabetic nephropathies [24]. Inflammasomes respond to a diverse range of pathogen-associated molecular patterns (PAMPs) and endogenously derived damage-associated molecular patterns (DAMPs) via a suite of pattern recognition receptors (PRR).…”

Section: The Nucleotide-binding Domain-like Receptor Protein 3 (Nlmentioning

confidence: 99%

“…Finally, as the pathogenesis of rhabdomyolysis is multifactorial, the role of other concomitant factors, acting either as priming stimuli or directly activating the NLRP3 inflammasome, should not be ignored. For instance, data from several studies suggest that different types of crystals, such as calcium oxalate, monosodium urate and cholesterol, can function as DAMPs to trigger NLRP3 inflammasome activation [22,25,83]. Recently, we highlighted a potential role for urate crystals in generating oxidative stress and activating the NLRP3 inflammasome in an animal model of rhabdomyolysis-associated AKI [10].…”

Section: Myoglobin-mediated Pigment Nephropathymentioning

confidence: 99%

Pigment Nephropathy: Novel Insights into Inflammasome-Mediated Pathogenesis

Giuliani

Kassianos

Healy

et al. 2019

IJMS

Self Cite

View full text Add to dashboard Cite

Pigment nephropathy is an acute decline in renal function following the deposition of endogenous haem-containing proteins in the kidneys. Haem pigments such as myoglobin and haemoglobin are filtered by glomeruli and absorbed by the proximal tubules. They cause renal vasoconstriction, tubular obstruction, increased oxidative stress and inflammation. Haem is associated with inflammation in sterile and infectious conditions, contributing to the pathogenesis of many disorders such as rhabdomyolysis and haemolytic diseases. In fact, haem appears to be a signalling molecule that is able to activate the inflammasome pathway. Recent studies highlight a pathogenic function for haem in triggering inflammatory responses through the activation of the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome. Among the inflammasome multiprotein complexes, the NLRP3 inflammasome has been the most widely characterized as a trigger of inflammatory caspases and the maturation of interleukin-18 and -1β. In the present review, we discuss the latest evidence on the importance of inflammasome-mediated inflammation in pigment nephropathy. Finally, we highlight the potential role of inflammasome inhibitors in the prophylaxis and treatment of pigment nephropathy.

show abstract

The Role of Oxidative Stress and Inflammation in Acute Oxalate Nephropathy Associated With Ethylene Glycol Intoxication

Cited by 7 publications

References 12 publications

Dietary Oxalate Intake and Kidney Outcomes

Dietary Oxalate Intake and Kidney Outcomes

Role of inflammation and inflammasome activation in human bile cast nephropathy

Pigment Nephropathy: Novel Insights into Inflammasome-Mediated Pathogenesis

Contact Info

Product

Resources

About