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Kidney International, ISSN 0085-2538, 06/2013, Volume 83, Issue 6, pp. 1029 - 1041
Oxidative stress and inflammation are mediators in the development and progression of chronic kidney disease (CKD) and its complications, and they are... 
ESRD | cardiovascular disease | CKD progression | inflammation | antioxidant therapy | oxidative stress | Oxidative stress | Cardiovascular disease | Antioxidant therapy | Inflammation | CYTOPROTECTIVE GENES | GLUTATHIONE SYNTHESIS | CARBON-MONOXIDE | AORTIC COARCTATION | REVERSE CHOLESTEROL TRANSPORT | BARDOXOLONE METHYL | CYCLOPENTENONE PROSTAGLANDINS | DENSITY-LIPOPROTEIN | UROLOGY & NEPHROLOGY | HEME OXYGENASE-1 | RENAL INJURY | Humans | Oleanolic Acid - analogs & derivatives | Kidney - immunology | NF-E2-Related Factor 2 - agonists | Renal Insufficiency, Chronic - drug therapy | Renal Insufficiency, Chronic - metabolism | Inflammation - metabolism | Kidney - metabolism | Time Factors | Inflammation - drug therapy | Renal Insufficiency, Chronic - diagnosis | Acute Kidney Injury - immunology | Inflammation - diagnosis | Oleanolic Acid - therapeutic use | Kidney Failure, Chronic - immunology | Kidney - drug effects | Renal Insufficiency, Chronic - immunology | Acute Kidney Injury - drug therapy | Kidney Failure, Chronic - drug therapy | Anti-Infective Agents - therapeutic use | Treatment Outcome | Inflammation - immunology | Disease Progression | Kidney Failure, Chronic - metabolism | Antioxidants - therapeutic use | Animals | NF-E2-Related Factor 2 - metabolism | Oxidative Stress - drug effects | Acute Kidney Injury - metabolism | bardoxolone methyl
Journal Article
Kidney International, ISSN 0085-2538, 03/2018, Volume 93, Issue 3, pp. 568 - 579
Renal tubules are the major component of the kidney and are vulnerable to a variety of injuries including hypoxia, proteinuria, toxins, metabolic disorders,... 
chronic kidney disease | acute kidney injury | renal fibrosis | renal tubule | renal inflammation | ACTIVATED PROTEIN-KINASE | CELL-CYCLE ARREST | GLOMERULAR EPITHELIAL-CELLS | ISCHEMIA-REPERFUSION INJURY | TO-MESENCHYMAL TRANSITION | TISSUE GROWTH-FACTOR | RENIN-ANGIOTENSIN SYSTEM | II-INDUCED HYPERTROPHY | UROLOGY & NEPHROLOGY | NF-KAPPA-B | PERICYTE-MYOFIBROBLAST TRANSITION | Cell Proliferation | Epithelial Cells - metabolism | Renal Insufficiency, Chronic - etiology | Humans | Renal Insufficiency, Chronic - metabolism | Acute Kidney Injury - complications | Epithelial-Mesenchymal Transition | Inflammation Mediators - metabolism | Acute Kidney Injury - immunology | Kidney Tubules - pathology | Kidney Tubules - metabolism | Cytokines - immunology | Inflammation Mediators - immunology | Kidney Tubules - immunology | Renal Insufficiency, Chronic - immunology | Cytokines - metabolism | Signal Transduction | Acute Kidney Injury - pathology | Cell Cycle Proteins - metabolism | Epithelial Cells - pathology | Immunity, Innate | Disease Progression | Renal Insufficiency, Chronic - pathology | Cell Cycle Checkpoints | Animals | Energy Metabolism | Epithelial Cells - immunology | Fibrosis | Acute Kidney Injury - metabolism | Senescence | Kidneys | Immune response | Mesenchyme | Epithelial cells | Inflammation | Epithelium | Drug development | Renal tubules | Cell death | Hypoxia | Metabolic disorders | Proteinuria
Journal Article
American Journal of Physiology - Lung Cellular and Molecular Physiology, ISSN 1040-0605, 2015, Volume 308, Issue 4, pp. L314 - L324
Sickle cell disease (SCD) is an autosomal recessive disorder in the gene encoding the beta -chain of hemoglobin. Deoxygenation causes the mutant hemoglobin S... 
Sickle cell disease | Nitric oxide | Pulmonary hypertension | Cell free hemoglobin | LACTATE-DEHYDROGENASE | nitric oxide | PHYSIOLOGY | pulmonary hypertension | NITRIC-OXIDE BIOAVAILABILITY | EXERCISE CAPACITY | KNOCKOUT MICE | sickle cell disease | cell free hemoglobin | ACUTE CHEST SYNDROME | RESPIRATORY SYSTEM | ARTERIAL-HYPERTENSION | FETAL-HEMOGLOBIN | TRANSGENIC MOUSE MODEL | PLATELET ACTIVATION | FREE HEMOGLOBIN | Humans | Heart Failure - physiopathology | Immunity, Innate - genetics | Oxidative Stress - immunology | Hypertension, Pulmonary - physiopathology | Acute Chest Syndrome - physiopathology | Hypertension, Pulmonary - therapy | Hemolysis - immunology | Renal Insufficiency, Chronic - therapy | Vascular Resistance - genetics | Heart Failure - immunology | Renal Insufficiency, Chronic - genetics | Reactive Oxygen Species - blood | Hemoglobin, Sickle - immunology | Toll-Like Receptor 4 - genetics | Vascular Diseases - genetics | Heart Failure - genetics | Toll-Like Receptor 4 - immunology | Renal Insufficiency, Chronic - physiopathology | Hemoglobin, Sickle - metabolism | Heme - immunology | Toll-Like Receptor 4 - blood | Nitric Oxide - genetics | Mutation | Vascular Diseases - blood | Practice Guidelines as Topic | Vascular Resistance - immunology | Heme - metabolism | Acute Chest Syndrome - therapy | Age Factors | Hypertension, Pulmonary - blood | Heart Failure - blood | Erythrocytes, Abnormal | Heart Failure - therapy | Heme - genetics | Reactive Oxygen Species - immunology | Acute Chest Syndrome - genetics | Acute Chest Syndrome - immunology | Hemolysis - genetics | Nitric Oxide - blood | Nitric Oxide - immunology | Vascular Diseases - immunology | Renal Insufficiency, Chronic - immunology | Vascular Diseases - therapy | Oxidative Stress - genetics | Hypertension, Pulmonary - genetics | Hypertension, Pulmonary - immunology | Hemoglobin, Sickle - genetics | Vascular Diseases - physiopathology | Renal Insufficiency, Chronic - blood | Acute Chest Syndrome - blood | Genetic aspects | Sickle cell anemia | Vasculitis | Diagnosis | Risk factors | Physiology in Medicine
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 09/2013, Volume 123, Issue 9, pp. 4023 - 4035
Journal Article
Kidney International, ISSN 0085-2538, 03/2018, Volume 93, Issue 3, pp. 656 - 669
Primary/secondary hyperoxalurias involve nephrocalcinosis-related chronic kidney disease (CKD) leading to end-stage kidney disease. Mechanistically, intrarenal... 
beta-hydroxybutyrate | necroinflammation | fibrosis | crystal nephropathy | NALP3 | OXALATE | REPAIR | DENDRITIC CELLS | RENAL INFLAMMATION | UROLOGY & NEPHROLOGY | MICROENVIRONMENTS | PROGRESSION | Cell Plasticity - drug effects | Inflammasomes - metabolism | Kidney - pathology | Nephrocalcinosis - immunology | Kidney - immunology | Hyperoxaluria - metabolism | Male | CARD Signaling Adaptor Proteins - genetics | Hyperoxaluria - drug therapy | NLR Family, Pyrin Domain-Containing 3 Protein - genetics | Renal Insufficiency, Chronic - metabolism | CARD Signaling Adaptor Proteins - metabolism | Kidney - metabolism | Nephrocalcinosis - metabolism | Butylene Glycols - pharmacology | Inflammasomes - drug effects | Interleukin-1 - immunology | Nephrocalcinosis - prevention & control | Female | Macrophages - immunology | Disease Models, Animal | Fibroblasts - metabolism | Interleukin-1 - metabolism | Renal Insufficiency, Chronic - immunology | Macrophages - pathology | Signal Transduction | NLR Family, Pyrin Domain-Containing 3 Protein - metabolism | Mice, Inbred C57BL | Cells, Cultured | NLR Family, Pyrin Domain-Containing 3 Protein - antagonists & inhibitors | Fibroblasts - pathology | Inflammasomes - genetics | Hyperoxaluria - pathology | Mice, Knockout | Renal Insufficiency, Chronic - pathology | Renal Insufficiency, Chronic - prevention & control | Macrophages - metabolism | Nephrocalcinosis - pathology | Phenotype | Animals | NLR Family, Pyrin Domain-Containing 3 Protein - immunology | Receptors, Transforming Growth Factor beta - metabolism | Inflammasomes - immunology | Fibroblasts - immunology | Macrophages - drug effects | Hyperoxaluria - immunology | End-stage renal disease | Phenotypes | CD11b antigen | Kidneys | Interleukin 1 receptor antagonist | Therapeutic applications | CX3CR1 protein | Inflammation | Macrophages | CD45 antigen | Atrophy | Signal transduction | Calcium oxalate | Oxalic acid | Calcinosis | Interleukin 1 | Fibrosis | Fibroblasts | Hyperoxaluria | Kidney diseases
Journal Article
Annals of the Rheumatic Diseases, ISSN 0003-4967, 06/2015, Volume 74, Issue 6, pp. 1178 - 1182
Objectives The RITUXVAS trial reported similar remission induction rates and safety between rituximab and cyclophosphamide based regimens for antineutrophil... 
MAINTENANCE | Cyclophosphamide | Treatment | ANTIBODY-ASSOCIATED VASCULITIS | THERAPY | Granulomatosis with polyangiitis | ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES | B cells | RHEUMATOLOGY | Systemic vasculitis | Azathioprine - therapeutic use | Glucocorticoids - therapeutic use | Renal Insufficiency, Chronic - etiology | Humans | Immunosuppressive Agents - therapeutic use | Middle Aged | Male | Microscopic Polyangiitis - complications | Cyclophosphamide - therapeutic use | Renal Insufficiency, Chronic - drug therapy | Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis - complications | Granulomatosis with Polyangiitis - immunology | Female | Microscopic Polyangiitis - immunology | Drug Therapy, Combination | B-Lymphocytes - cytology | Renal Insufficiency, Chronic - immunology | Rituximab | Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis - drug therapy | Disease Progression | Disease-Free Survival | Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis - immunology | Lymphocyte Count | Microscopic Polyangiitis - drug therapy | Granulomatosis with Polyangiitis - drug therapy | Aged | Antibodies, Monoclonal, Murine-Derived - therapeutic use | Granulomatosis with Polyangiitis - complications | Kidney Failure, Chronic - etiology | Usage | Care and treatment | Vasculitis | Patient outcomes | Clinical trials | Dosage and administration | Comparative analysis | Risk factors | Clinical Medicine | Medical and Health Sciences | Klinisk medicin | B cells; Cyclophosphamide; Granulomatosis with polyangiitis; Systemic vasculitis; Treatment | Medicin och hälsovetenskap
Journal Article