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Aristolochic acid nephropathy

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https://www.readbyqxmd.com/read/27892830/risk-assessment-of-plant-food-supplements-and-other-herbal-products-containing-aristolochic-acids-using-the-margin-of-exposure-moe-approach
#1
Rozaini Abdullah, Leolean Nyle Diaz, Sebastiaan Wesseling, Ivonne M C M Rietjens
After the incidences of induction of Aristolochic Acid Nephropathy after consumption of herbal weight loss preparations that accidentally contained aristolochic acids (AAs), several countries defined national restrictions on the presence of AAs in food, including plant food supplements (PFS) and herbal products. The aim of the present study was to investigate whether the risks associated with exposure to AAs via PFS and herbal products are at present indeed negligible. Data reported in literature on AA levels in PFS and other herbal products and also obtained from a new series of PFS in the present study were used to calculate the estimated daily intakes (EDIs) and corresponding Margin of Exposure (MOE) values...
November 28, 2016: Food Additives & Contaminants. Part A, Chemistry, Analysis, Control, Exposure & Risk Assessment
https://www.readbyqxmd.com/read/27785421/lynch-syndrome-and-exposure-to-aristolochic-acid-in-upper-tract-urothelial-carcinoma-its-clinical-impact
#2
REVIEW
Pierre Colin, Thomas Seisen, Romain Mathieu, Sharohkh F Shariat, Morgan Rouprêt
The purpose of the current review was to describe the clinical risk for Lynch syndrome (LS) after exposure to aristolochic acid (AA) in cases of upper urinary-tract urothelial carcinoma (UTUC). A systematic review of the scientific literature was performed using the Medline database (National Library of Medicine, PubMed) using the following keywords: epidemiology, risk factor, AA, Balkan nephropathy (BNe), LS, hereditary cancer, hereditary non-polyposis colorectal cancer (HNPCC), mismatch repair genes, urothelial carcinomas, upper urinary tract, renal pelvis, ureter, Amsterdam criteria, genetic counselling, mismatch repair genes, genetic instability, microsatellite, and Bethesda guidelines...
October 2016: Translational Andrology and Urology
https://www.readbyqxmd.com/read/27763560/renal-protective-effects-of-17%C3%AE-estradiol-on-mice-with-acute-aristolochic-acid-nephropathy
#3
Min Shi, Liang Ma, Li Zhou, Ping Fu
Aristolochic acid nephropathy (AAN) is a progressive kidney disease caused by a Chinese herb containing aristolochic acid. Excessive death of renal tubular epithelial cells (RTECs) characterized the acute phase of AAN. Therapies for acute AAN were limited, such as steroids and angiotensin-receptor blockers (ARBs)/angiotensin-converting enzyme inhibitors (ACEIs). It was interesting that, in acute AAN, female patients showed relative slower progression to renal failure than males. In a previous study, female hormone 17β-estradiol (E2) was found to attenuate renal ischemia-reperfusion injury...
October 18, 2016: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/27750081/metabolomics-insights-into-activated-redox-signaling-and-lipid-metabolism-dysfunction-in-chronic-kidney-disease-progression
#4
Hua Chen, Gang Cao, Dan-Qian Chen, Ming Wang, Nosratola D Vaziri, Zhi-Hao Zhang, Jia-Rong Mao, Xu Bai, Ying-Yong Zhao
Early detection is critical in prevention and treatment of kidney disease. However currently clinical laboratory and histopathological tests do not provide region-specific and accurate biomarkers for early detection of kidney disease. The present study was conducted to identify sensitive biomarkers for early detection and progression of tubulo-interstitial nephropathy in aristolochic acid I-induced rats at weeks 4, 8 and 12. Biomarkers were validated using aristolochic acid nephropathy (AAN) rats at week 24, adenine-induced chronic kidney disease (CKD) rats and CKD patients...
September 28, 2016: Redox Biology
https://www.readbyqxmd.com/read/27716846/omeprazole-alleviates-aristolochia-manshuriensis-kom-induced-acute-nephrotoxicity
#5
Lianmei Wang, Hongbing Zhang, Chunying Li, Yan Yi, Jing Liu, Yong Zhao, Jingzhuo Tian, Yushi Zhang, Xiaolu Wei, Yue Gao, Aihua Liang
Aristolochia manshuriensis Kom (AMK) is a member of the Aristolochiaceae family and is a well-known cause of aristolochic acid (AA) nephropathy. In this study, we investigated the potential of omeprazole (OM) to alleviate AMK-induced nephrotoxicity. We found that OM reduced mouse mortality caused by AMK and attenuated AMK-induced acute nephrotoxicity in rats. OM enhanced hepatic Cyp 1a1/2 and renal Cyp 1a1 expression in rats, as well as CYP 1A1 expression in human renal tubular epithelial cells (HKCs). HKCs with ectopic CYP 1A1 expression were more tolerant to AA than the control cells...
2016: PloS One
https://www.readbyqxmd.com/read/27557898/impact-of-genetic-modulation-of-sult1a-enzymes-on-dna-adduct-formation-by-aristolochic-acids-and-3-nitrobenzanthrone
#6
Volker M Arlt, Walter Meinl, Simone Florian, Eszter Nagy, Frantisek Barta, Marlies Thomann, Iveta Mrizova, Annette M Krais, Maggie Liu, Meirion Richards, Amin Mirza, Klaus Kopka, David H Phillips, Hansruedi Glatt, Marie Stiborova, Heinz H Schmeiser
Exposure to aristolochic acid (AA) causes aristolochic acid nephropathy (AAN) and Balkan endemic nephropathy (BEN). Conflicting results have been found for the role of human sulfotransferase 1A1 (SULT1A1) contributing to the metabolic activation of aristolochic acid I (AAI) in vitro. We evaluated the role of human SULT1A1 in AA bioactivation in vivo after treatment of transgenic mice carrying a functional human SULT1A1-SULT1A2 gene cluster (i.e. hSULT1A1/2 mice) and Sult1a1(-/-) mice with AAI and aristolochic acid II (AAII)...
August 24, 2016: Archives of Toxicology
https://www.readbyqxmd.com/read/27538407/balkan-endemic-nephropathy-an-update-on-its-aetiology
#7
Marie Stiborová, Volker M Arlt, Heinz H Schmeiser
Balkan endemic nephropathy (BEN) is a unique, chronic renal disease frequently associated with upper urothelial cancer (UUC). It only affects residents of specific farming villages located along tributaries of the Danube River in Bosnia-Herzegovina, Croatia, Macedonia, Serbia, Bulgaria, and Romania where it is estimated that ~100,000 individuals are at risk of BEN, while ~25,000 have the disease. This review summarises current findings on the aetiology of BEN. Over the last 50 years, several hypotheses on the cause of BEN have been formulated, including mycotoxins, heavy metals, viruses, and trace-element insufficiencies...
November 2016: Archives of Toxicology
https://www.readbyqxmd.com/read/27536690/autophagy-in-chronic-kidney-diseases
#8
REVIEW
Na Liu, Yingfeng Shi, Shougang Zhuang
BACKGROUND: Autophagy is the degrading process of protein and organelles mediated by lysosomes. This process is involved in purging senescent organelles and subversive proteins while maintaining the stability of the intracellular environment. This phenomenon is highly conservative, existing in nearly every species, and is involved in cell growth, proliferation and tumorigenesis. SUMMARY: In recent decades, with the discovery of autophagy-related genes and proteins in conjunction with the improvement in detection methods, the study of autophagy is constantly achieving new breakthroughs...
April 2016: Kidney Diseases
https://www.readbyqxmd.com/read/27508743/-op-5b-09-aristolochic-acid-nephropathy-a-case-of-slower-vascular-aging
#9
V Premuzc, V Ivkovic, N Leko, Z Stipancic, T Teskera, M Vinkovic, M Barisic, S Karanovic, A Vrdoljak, I Vukovic, Z Dika, M Laganovic, B Jelakovic
OBJECTIVE: Early vascular aging (EVA) is a feature of chronic kidney disease(CKD) and pulse wave velocity(PWV) is independent predictor of premature cardiovascular(CV) mortality. High blood pressure(BP) and vascular calcifications contribute mostly to EVA in this group. Endemic nephropathy(EN), an environmental form of aristolochic acid nephropathy, is a chronic tubulointerstitial salt wasting nephropathy characterized with later onset and milder forms of hypertension (HT), and in line with this we hypothesized that arterial stiffness progresses slowlier in EN pts resulting in lower CV mortality...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27418141/bioinformatics-facilitating-the-use-of-microarrays-to-delineate-potential-mirna-biomarkers-in-aristolochic-acid-nephropathy
#10
Yana Lv, Yumei Que, Qiao Su, Qiang Li, Xi Chen, Haitao Lu
Aristolochic acid nephropathy (AAN) is a rapidly progressive acute or chronic tubulointerstitial nephritis (TIN). The present study attempted to explore the molecular mechanisms underlying the miRNA-directed development of AAN. Our differentially expressed analysis identified 11 DE-miRNAs and retrieved the target genes of these DE-miRNAs; then, network analysis and functional analysis further identified 6 DE-miRNAs (has-miR-192, has-miR-194, has-miR-542-3p, has-miR-450a, has-miR-584, has-miR-33a) as phenotypic biomarkers of AAN...
July 13, 2016: Oncotarget
https://www.readbyqxmd.com/read/27379382/blocking-tgf-%C3%AE-signaling-pathway-preserves-mitochondrial-proteostasis-and-reduces-early-activation-of-pdgfr%C3%AE-pericytes-in-aristolochic-acid-induced-acute-kidney-injury-in-wistar-male-rats
#11
Agnieszka A Pozdzik, Laetitia Giordano, Gang Li, Marie-Hélène Antoine, Nathalie Quellard, Julie Godet, Eric De Prez, Cécile Husson, Anne-Emilie Declèves, Volker M Arlt, Jean-Michel Goujon, Isabelle Brochériou-Spelle, Steven R Ledbetter, Nathalie Caron, Joëlle L Nortier
BACKGROUND: The platelet-derived growth factor receptor β (PDGFRβ)+ perivascular cell activation becomes increasingly recognized as a main source of scar-associated kidney myofibroblasts and recently emerged as a new cellular therapeutic target. AIMS: In this regard, we first confirmed the presence of PDGFRβ+ perivascular cells in a human case of end-stage aristolochic acid nephropathy (AAN) and thereafter we focused on the early fibrosis events of transforming growth factor β (TGFβ) inhibition in a rat model of AAN...
2016: PloS One
https://www.readbyqxmd.com/read/27362729/quantitation-of-aristolochic-acids-in-corn-wheat-grain-and-soil-samples-collected-in-serbia-identifying-a-novel-exposure-pathway-in-the-etiology-of-balkan-endemic-nephropathy
#12
Wan Chan, Nikola M Pavlović, Weiwei Li, Chi-Kong Chan, Jingjing Liu, Kailin Deng, Yinan Wang, Biljana Milosavljević, Emina N Kostić
While to date investigations provided convincing evidence on the role of aristolochic acids (AAs) in the etiology of Balkan endemic nephropathy (BEN) and upper urothelial cancer (UUC), the exposure pathways by which AAs enter human bodies to cause BEN and UUC remain obscure. The goal of this study is to test the hypothesis that environmental pollution by AAs and root uptake of AAs in the polluted soil may be one of the pathways by which AAs enter the human food chain. The hypothesis driving this study was that the decay of Aristolochia clematitis L...
July 27, 2016: Journal of Agricultural and Food Chemistry
https://www.readbyqxmd.com/read/27352112/expression-of-renal-aquaporins-in-aristolochic-acid-i-and-aristolactam-i-induced-nephrotoxicity
#13
Ji Li, Liang Zhang, ZhenZhou Jiang, XiuQin He, LuYong Zhang, Ming Xu
BACKGROUND: Exposure to aristolochic acid (AA) can cause AA nephropathy, which is characterized by extensive proximal tubular damage and polyuria. METHODS: To test the hypothesis that polyuria might be induced by altered regulation of aquaporins (AQPs) in the kidney, different doses of AA-I or aristolactam I (AL-I) were administered intraperitoneally to Sprague-Dawley rats, and urine, blood, and kidney samples were analyzed. In addition, AQP1, AQP2, AQP4 and AQP6 expression in the kidney were determined...
2016: Nephron
https://www.readbyqxmd.com/read/27328942/loss-of-expression-of-protein-phosphatase-magnesium-dependent-1a-during-kidney-injury-promotes-fibrotic-maladaptive-repair
#14
Rohan Samarakoon, Alexandra Rehfuss, Nidah S Khakoo, Lucas L Falke, Amy D Dobberfuhl, Sevann Helo, Jessica M Overstreet, Roel Goldschmeding, Paul J Higgins
Protein phosphatase magnesium-dependent-1A (PPM1A) dephosphorylates SMAD2/3, which suppresses TGF-β signaling in keratinocytes and during Xenopus development; however, potential involvement of PPM1A in chronic kidney disease is unknown. PPM1A expression was dramatically decreased in the tubulointerstitium in obstructive and aristolochic acid nephropathy, which correlates with progression of fibrotic disease. Stable silencing of PPM1A in human kidney-2 human renal epithelial cells increased SMAD3 phosphorylation, stimulated expression of fibrotic genes, induced dedifferentiation, and orchestrated epithelial cell-cycle arrest via SMAD3-mediated connective tissue growth factor and plasminogen activator inhibitor-1 up-regulation...
October 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/27267499/reduced-rat-plasma-lysophosphatidylglycerol-or-lysophosphatidic-acid-level-as-a-biomarker-of-aristolochic-acid-induced-renal-and-adipose-dysfunctions
#15
Toshihiko Tsutsumi, Yoko Okamoto, Syougo Yamakawa, Cheng Bingjun, Akira Ishihara, Tamotsu Tanaka, Akira Tokumura
AIMS: Food products and diet pills containing aristolochic acid (AA) are responsible for a rapid progression of nephropathy associated with reduced body weight in human beings. In this study, we investigated the relationship of dietary NaCl and lysophospholipid (LPL) plasma levels to body weight gain in AA-treated rats. MAIN METHODS: Male rats receiving a salt-deficient chow, normal salt chow or high salt chow were injected intraperitoneally daily with AA for 15days...
July 15, 2016: Life Sciences
https://www.readbyqxmd.com/read/27237586/mutational-signature-of-aristolochic-acid-clue-to-the-recognition-of-a-global-disease
#16
REVIEW
Thomas A Rosenquist, Arthur P Grollman
Mutational signatures associated with specific forms of DNA damage have been identified in several forms of human cancer. Such signatures provide information regarding mechanisms of tumor induction which, in turn, can reduce exposure to carcinogens by shaping public health policy. Using a molecular epidemiologic approach that takes advantage of recent advances in genome sequencing while applying sensitive and specific analytical methods to characterize DNA damage, it has become increasingly possible to establish causative linkages between certain environmental mutagens and disease risk...
August 2016: DNA Repair
https://www.readbyqxmd.com/read/27218105/microrna-profiling-in-patients-with-upper-tract-urothelial-carcinoma-associated-with-balkan-endemic-nephropathy
#17
Katerina Popovska-Jankovic, Predrag Noveski, Ljubinka Jankovic-Velickovic, Slavica Stojnev, Rade Cukuranovic, Vladisav Stefanovic, Draga Toncheva, Rada Staneva, Momir Polenakovic, Dijana Plaseska-Karanfilska
Balkan endemic nephropathy (BEN) is a disease that affects people that live in the alluvial plains along the tributaries of the Danube River in the Balkan region. BEN is a chronic tubulointerstitial disease with a slow progression to terminal renal failure and has strong association with upper tract urothelial carcinoma (UTUC). There are several hypotheses about the etiology of BEN, but only the toxic effect of aristolochic acid has been confirmed as a risk factor in the occurrence of the disease. Aberrantly expressed miRNAs have been shown to be associated with many types of cancers...
2016: BioMed Research International
https://www.readbyqxmd.com/read/26914156/aristolochic-acid-a-plant-extract-used-in-the-treatment-of-pain-and-linked-to-balkan-endemic-nephropathy-is-a-regulator-of-k2p-channels
#18
Emma L Veale, Alistair Mathie
BACKGROUND AND PURPOSE: Aristolochic acid (AristA) is found in plants used in traditional medicines to treat pain. We investigated the action of AristA on TREK and TRESK, potassium (K2P) channels, which are potential therapeutic targets in pain. Balkan endemic nephropathy (BEN) is a renal disease associated with AristA consumption. A mutation of TASK-2 (K2P 5.1) channels (T108P) is seen in some patients susceptible to BEN, so we investigated how both this mutation and AristA affected TASK-2 channels...
May 2016: British Journal of Pharmacology
https://www.readbyqxmd.com/read/26909597/targeting-c-fms-kinase-attenuates-chronic-aristolochic-acid-nephropathy-in-mice
#19
Xiao Y Dai, Xiao R Huang, Li Zhou, Lin Zhang, Ping Fu, Carl Manthey, David J Nikolic-Paterson, Hui Y Lan
Aristolochic acid nephropathy (AAN) is a progressive kidney disease caused by some Chinese herbal medicines, but treatment remains ineffective. Macrophage accumulation is an early feature in human and experimental AAN; however, the role of macrophages in chronic AAN is unknown. We report here that targeting macrophages with fms-I, a selective inhibitor of the tyrosine kinase activity of the macrophage colony-stimulating factor receptor, suppressed disease progression in a mouse model of chronic AAN. Treatment with fms-I (10mg/kg/BID) from day 0 to 28 (prevention study) or from day 14 to 28 (intervention study) substantially inhibited macrophage accumulation and significantly improved renal dysfunction including a reduction in proteinuria and tubular damage...
March 8, 2016: Oncotarget
https://www.readbyqxmd.com/read/26861298/active-site-mutations-as-a-suitable-tool-contributing-to-explain-a-mechanism-of-aristolochic-acid-i-nitroreduction-by-cytochromes-p450-1a1-1a2-and-1b1
#20
Jan Milichovský, František Bárta, Heinz H Schmeiser, Volker M Arlt, Eva Frei, Marie Stiborová, Václav Martínek
UNLABELLED: Aristolochic acid I (AAI) is a plant drug found in Aristolochia species that causes aristolochic acid nephropathy, Balkan endemic nephropathy and their associated urothelial malignancies. AAI is activated via nitroreduction producing genotoxic N-hydroxyaristolactam, which forms DNA adducts. The major enzymes responsible for the reductive bioactivation of AAI are NAD(P)H: quinone oxidoreductase and cytochromes P450 (CYP) 1A1 and 1A2. Using site-directed mutagenesis we investigated the possible mechanisms of CYP1A1/1A2/1B1-catalyzed AAI nitroreduction...
February 5, 2016: International Journal of Molecular Sciences
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