Progression after AKI: Understanding Maladaptive Repair Processes to Predict and Identify Therapeutic Treatments. - sprookjes - yvandenbroek - TriplyDB

Progression after AKI: Understanding Maladaptive Repair Processes to Predict and Identify Therapeutic Treatments.

Progression after AKI: Understanding Maladaptive Repair Processes to Predict and Identify Therapeutic Treatments.

http://www.wikidata.org/entity/Q30278441

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The proximal tubule is the primary target of injury and progression of kidney disease: role of the glomerulotubular junction.Lack of an apparent role for endothelin-1 in the prolonged reduction in renal perfusion following severe unilateral ischemia-reperfusion injury in the mouse.Human adipose stromal cell therapy improves survival and reduces renal inflammation and capillary rarefaction in acute kidney injury.Bridging translation for acute kidney injury with better preclinical modeling of human disease PROGRESSION OF CHRONIC KIDNEY DISEASE AFTER ACUTE KIDNEY INJURY.Vitamin D deficiency contributes to vascular damage in sustained ischemic acute kidney injury.Human CD133(+) Renal Progenitor Cells Induce Erythropoietin Production and Limit Fibrosis After Acute Tubular Injury.Renal recovery after acute kidney injury DNA methylation protects against cisplatin-induced kidney injury by regulating specific genes, including interferon regulatory factor 8.Stop adding insult to injury-identifying and managing risk factors for the progression of acute kidney injury in children.Targeting the KEAP1-NRF2 System to Prevent Kidney Disease Progression.Biomarkers for the Early Detection and Prognosis of Acute Kidney Injury.Cellular plasticity in kidney injury and repair.Metabolic reprogramming and tolerance during sepsis-induced AKI.Differences in acute kidney injury ascertainment for clinical and preclinical studies.Endothelial colony-forming cells and pro-angiogenic cells: clarifying definitions and their potential role in mitigating acute kidney injury.Keap1 hypomorphism protects against ischemic and obstructive kidney disease Acute interstitial nephritis in the south of Iran; an observational study Molecular characterization of the transition from acute to chronic kidney injury following ischemia/reperfusion.Evolutionary Nephrology.Targeting neural reflex circuits in immunity to treat kidney disease.Mitochondria Protection after Acute Ischemia Prevents Prolonged Upregulation of IL-1β and IL-18 and Arrests CKD.Antithrombin III prevents progression of chronic kidney disease following experimental ischaemic-reperfusion injury.Recent advances in the pathogenetic mechanisms of sepsis-associated acute kidney injury.Th17 cells contribute to pulmonary fibrosis and inflammation during chronic kidney disease progression following acute ischemia.New Ultrasound Techniques Promise Further Advances in AKI and CKD.Accounting for oxygen in the renal cortex: a computational study of factors that predispose the cortex to hypoxia.Cystatin C predicts acute kidney injury and mortality in cirrhotics: A prospective cohort study.Reducing Inflammatory Cytokine Production from Renal Collecting Duct Cells by Inhibiting GATA2 Ameliorates Acute Kidney Injury.Renal hypoxia in kidney disease: Cause or consequence?AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms.Breast Regression Protein-39/Chitinase 3-Like 1 Promotes Renal Fibrosis after Kidney Injury via Activation of Myofibroblasts.Lymphocyte-specific deletion of IKK2 or NEMO mediates an increase in intrarenal Th17 cells and accelerates renal damage in an ischemia-reperfusion injury mouse model.Genome-wide analysis revealed that DZNep reduces tubulointerstitial fibrosis via down-regulation of pro-fibrotic genes.Overcoming Translational Barriers in Acute Kidney Injury: A Report from an NIDDK Workshop.Acute Kidney Injury as a Condition of Renal Senescence.Nitrolipids in kidney physiology and disease.Acute Kidney Injury and Progression of Diabetic Kidney Disease.Preventing the Progression of AKI to CKD: The Role of Mitochondria.Persistent expression of neutrophil gelatinase-associated lipocalin and M2 macrophage markers and chronic fibrosis after acute kidney injury.

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Progression after AKI: Understanding Maladaptive Repair Processes to Predict and Identify Therapeutic Treatments.

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2015 nî lūn-bûn

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2015 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2015 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2015年の論文

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Progression after AKI: Underst ...... entify Therapeutic Treatments.

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ADQI XIII Work Group

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David P Basile

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John A Kellum

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Joseph V Bonventre

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Masaomi Nangaku

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Robert Unwin

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P2860

AKI transition of care: a potential opportunity to detect and prevent CKD

Epigenetics of progression of chronic kidney disease: fact or fantasy?

Hypoxia-inducible factors in the kidney

Severe renal mass reduction impairs recovery and promotes fibrosis after AKI

Dysregulated nephrin in diabetic nephropathy of type 2 diabetes: a cross sectional study

Evidence that fibroblasts derive from epithelium during tissue fibrosis

Therapeutic Targets of Human AKI: Harmonizing Human and Animal AKI

Potential use of biomarkers in acute kidney injury: report and summary of recommendations from the 10th Acute Dialysis Quality Initiative consensus conference.

Magnetic resonance elastography noninvasively detects in vivo renal medullary fibrosis secondary to swine renal artery stenosis

Inhibition of autoregulated TGFbeta signaling simultaneously enhances proliferation and differentiation of kidney epithelium and promotes repair following renal ischemia.

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3

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Mitchell H. Rosner

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