scholarly journals MP097L-ARGININE SUPPLEMENTATION IMPROVES CHRONIC KIDNEY INJURY IN EXPERIMENTAL ARISTOLOCHIC ACID NEPHROPATHY

2016 ◽  
Vol 31 (suppl_1) ◽  
pp. i374-i374
Author(s):  
Inès Jadot ◽  
Vanessa Colombaro ◽  
Blanche Martin ◽  
Isabelle Habsch ◽  
Olivia Botton ◽  
...  
Keyword(s):  
Aristolochic Acid ◽  
Kidney Injury ◽  
Aristolochic Acid Nephropathy ◽  
Chronic Kidney Injury ◽  
Arginine Supplementation

scholarly journals Macrophages-Derived, LRG1-Enriched Extracellular Vesicles Exacerbate Aristolochic Acid Nephropathy Via A TGFβR1-Dependent Manner

2021 ◽  
Author(s):  
Wenjuan Jiang ◽  
Jiahui Dong ◽  
Changlin Du ◽  
Chuanting Xu ◽  
Songbing Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aristolochic Acid ◽  
Herbal Medicines ◽  
Kidney Injury ◽  
Dependent Manner ◽  
Aristolochic Acid Nephropathy ◽  
Injury Model ◽  
Culture Model

Abstract Aristolochic acid nephropathy (AAN) is a progressive kidney disease caused by some herbal medicines, but treatment remains ineffective. We previously found NADPH oxidases 4 (NOX4), which regulates oxidative stress, play an important role in kidney injury model. However, its regulatory mechanism of action in AAN is still obscure. In this study, we established AAN model in vivo, a co-culture system of macrophage and TEC, and macrophage/TEC conditioned media culture model in vitro respectively. We found macrophages infiltration promoted injury，oxidative stress and apoptosis of TEC. Furthermore, the role of macrophage in AAN was dependent on macrophages-derived EV. Importantly, we found that macrophages-derived, Leucine-rich α-2-glycoprotein 1(LRG1)-enriched EV induced TEC injury and apoptosis of via a TGFβR1-dependent process. Mechanistically, macrophages-derived, LRG1-enriched EV mediating TECs injury by upregulating NOX4 in AAN model. This study may help design a better therapeutic strategy to treat AAN patients.

scholarly journals Mesenchymal Stem Cell Derived Extracellular Vesicles Ameliorate Kidney Injury in Aristolochic Acid Nephropathy

2020 ◽  
Vol 8 ◽  
Author(s):  
Sharad Kholia ◽  
Maria Beatriz Herrera Sanchez ◽  
Massimo Cedrino ◽  
Elli Papadimitriou ◽  
Marta Tapparo ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Extracellular Vesicles ◽  
Aristolochic Acid ◽  
Kidney Injury ◽  
Aristolochic Acid Nephropathy

Enzymes Metabolizing Aristolochic Acid and their Contribution to the Development of Aristolochic Acid Nephropathy and Urothelial Cancer

2013 ◽  
Vol 14 (6) ◽  
pp. 695-705 ◽  
Author(s):  
Marie Stiborova ◽  
Vaclav Martínek ◽  
Eva Frei ◽  
Volker Arlt ◽  
Heinz Schmeiser
Keyword(s):  
Urothelial Cancer ◽  
Aristolochic Acid ◽  
Aristolochic Acid Nephropathy

scholarly journals The Macrophage Phagocytic Receptor CD36 Promotes Fibrogenic Pathways on Removal of Apoptotic Cells during Chronic Kidney Injury

2015 ◽  
Vol 185 (8) ◽  
pp. 2232-2245 ◽  
Author(s):  
Subramaniam Pennathur ◽  
Katie Pasichnyk ◽  
Nadia M. Bahrami ◽  
Lixia Zeng ◽  
Maria Febbraio ◽  
...  
Keyword(s):  
Kidney Injury ◽  
Apoptotic Cells ◽  
Chronic Kidney Injury

Metastatische pulmonale calcificaties als zeldzame oorzaak van matglasopaciteiten op een CT-scan

2021 ◽  
Author(s):  
I. CARPENTIER ◽  
E. PEETERS ◽  
B. VANZIELEGHEM
Keyword(s):  
Correct Diagnosis ◽  
Kidney Injury ◽  
Lung Damage ◽  
Ground Glass ◽  
Literature Overview ◽  
Chronic Kidney Injury ◽  
Patient’S History ◽  
Pulmonary Calcifications ◽  
Metastatic Pulmonary Calcification

Metastatic pulmonary calcification: a case report and literature overview Ground-glass opacities have a broad differential diagnosis, including infectious, metabolic, inflammatory and malignant causes. This case presents an underdiagnosed entity of dense ground-glass opacities, namely metastatic pulmonary calcifications (MPC). This is a benign metabolic disease characterised by the deposition of calcium in the lungs, mostly described in patients with chronic kidney injury and secondary hyperparathyroidism. The majority of the patients require no treatment, but in some cases it may lead to irreversible lung damage. Clinical and radiological features, as well as the patient’s history, are crucial to make a correct diagnosis since MPC has a relatively specific appearance on imaging. This case study discusses the medical history and imaging appearance of a 44-year-old woman with MPC, followed by a literature overview.

scholarly journals Urinary angiotensinogen as a biomarker for acute to chronic kidney injury transition – prognostic and mechanistic implications

2018 ◽  
Vol 132 (21) ◽  
pp. 2383-2385 ◽  
Author(s):  
Katie L. Connor ◽  
Laura Denby
Keyword(s):  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Ischaemia Reperfusion Injury ◽  
Angiotensin System ◽  
Urinary Angiotensinogen ◽  
Tubular Necrosis ◽  
Ischaemia Reperfusion ◽  
Structural Recovery ◽  
Chronic Kidney Injury ◽  
Injury Model

Accurate biomarkers that both predict the progression to, and detect the early stages of chronic kidney disease (CKD) are lacking, resulting in difficulty in identifying individuals who could potentially benefit from targeted intervention. In a recent issue [Clinical Science (2018) 132, 2121–2133], Cui et al. examine the ability of urinary angiotensinogen (uAGT) to predict the progression of acute kidney injury (AKI) to CKD. They principally employ a murine ischaemia reperfusion injury model to study this and provide data from a small prospective study of patients with biopsy proven acute tubular necrosis. The authors suggest that uAGT is a dynamic marker of renal injury that could be used to predict the likelihood of structural recovery following AKI. Here we comment on their findings, exploring the clinical utility of uAGT as a biomarker to predict AKI to CKD transition and perhaps more controversially, to discuss whether the early renin–angiotensin system blockade following AKI represents a therapeutic target.

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