Associate Professor, Medicine, University of Colorado School of Medicine
Nephrology
Dr. Sarah Faubel, MD
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Doctor Sarah Faubel, MD is an expert in the field of Nephrology. She attended Wayne State University School of Medicine. Wayne State University School of Medicine has a rank of 63 in research and a 85 in primary care Sarah Faubel is a published doctor. She has 59 publications published. The most current publication "Delivery of interleukin-10 via injectable hydrogels improves renal outcomes and reduces systemic inflammation following ischemic acute kidney injury in mice." She accepts all Medicare patients.
Publications
- Delivery of interleukin-10 via injectable hydrogels improves renal outcomes and reduces systemic inflammation following ischemic acute Kidney injury in mice.
- A Decline in Intraoperative Renal Near-Infrared Spectroscopy Is Associated With Adverse Outcomes in Children Following Cardiac Surgery.
- Bridging Translation by Improving Preclinical Study Design in AKI.
- Outpatient Dialysis for Patients with AKI: A Policy Approach to Improving Care.
- Local immunotherapy via delivery of interleukin-10 and transforming growth factor β antagonist for treatment of Chronic kidney disease.
- Dual therapy difficulties in Angiotensin blockade for proteinuria: a teachable moment.
- The Daily Burden of Acute Kidney Injury: A Survey of US Nephrologists on World Kidney Day.
- Renal relevant radiology: introduction.
- Have we reached the limit of mortality benefit with our approach to renal replacement therapy in acute Kidney injury?
- Heparanase mediates Renal dysfunction during early sepsis in mice.
- Renal Relevant Radiology: Use of Ultrasonography in Patients with AKI.
- Obesity development in caspase-1-deficient mice.
- AKI Transition of Care: A Potential Opportunity to Detect and Prevent CKD.
- Endocytosis of albumin by podocytes elicits an inflammatory response and induces apoptotic cell death.
- Urine IL-18, NGAL, IL-8 and serum IL-8 are biomarkers of acute Kidney injury following liver transplantation.
- Circulating IL-6 mediates lung injury via CXCL1 production after acute Kidney injury in mice.
- Cytokine production increases and cytokine clearance decreases in mice with bilateral nephrectomy.
- Complement activation and toll-like receptor-2 signaling contribute to cytokine production after Renal ischemia/reperfusion.
- Ongoing Clinical Trials in AKI.
- Preparing for renal replacement therapy in patients with the ebola virus Disease.
- Acute Lung Injury and Acute Kidney Injury Are Established by Four Hours in Experimental Sepsis and Are Improved with Pre, but Not Post, Sepsis Administration of TNF-α ...
- Intratracheal IL-6 Protects against Lung Inflammation in Direct, but Not Indirect, Causes of Acute Lung Injury in Mice.
- Depletion of Macrophages and Dendritic Cells in Ischemic Acute Kidney Injury.
- Macrophages mediate lung inflammation in a mouse model of ischemic acute Kidney injury.
- Acute Kidney injury: Severity of illness scoring systems in acute Kidney injury.
- IL-33 exacerbates acute Kidney injury.
- In critically ill patients requiring CRRT, AKI is associated with increased respiratory failure and death versus ESRD.
- Cytokines in acute Kidney injury (AKI).
- Age and Gender Dimorphisms Contribute to the Severity of Bleomycin-Induced Lung Injury and Fibrosis.
- Splenectomy exacerbates lung injury after ischemic acute Kidney injury in mice.
- Apoptosis and autophagy in cold preservation ischemia.
- Urine interleukin-6 is an early biomarker of acute Kidney injury in children undergoing cardiac surgery.
- Acute Kidney injury and multiple organ dysfunction syndrome.
- Serum interleukin-6 and interleukin-8 are early biomarkers of acute Kidney injury and predict prolonged mechanical ventilation in children undergoing cardiac surgery: ...
- Macrophages are not the source of injurious interleukin-18 in ischemic acute Kidney injury in mice.
- Interleukin-18 binding protein transgenic mice are protected against ischemic acute Kidney injury.
- Role of NF-kappaB and PI 3-kinase/Akt in TNF-alpha-induced cytotoxicity in microvascular endothelial cells.
- Interleukin-6 mediates lung injury following ischemic acute Kidney injury or bilateral nephrectomy.
- Pulmonary complications after acute Kidney injury.
- Exciting times in research regarding the definition, diagnosis, complications, and outcomes of acute Kidney injury.
- Endotoxemia-related acute Kidney injury in transgenic mice with endothelial overexpression of GTP cyclohydrolase-1.
- Fractalkine receptor (CX3CR1) inhibition is protective against ischemic acute Renal failure in mice.
- Increased macrophage infiltration and fractalkine expression in cisplatin-induced acute Renal failure in mice.
- VEGF receptor inhibition slows the progression of polycystic Kidney disease.
- Cisplatin-induced acute renal failure is associated with an increase in the cytokines interleukin (IL)-1beta, IL-18, IL-6, and neutrophil infiltration in the Kidney.
- Proximal tubules from caspase-1-deficient mice are protected against hypoxia-induced membrane injury.
- Acute Renal failure after bilateral nephrectomy is associated with cytokine-mediated pulmonary injury.
- Caspases and calpain are independent mediators of cisplatin-induced endothelial cell necrosis.
- Ischemic acute Renal failure following nephrectomy impairs long-term Renal function.
- Caspases as drug targets in ischemic organ injury.
- Peripheral CD4 T-cell depletion is not sufficient to prevent ischemic acute Renal failure.
- Caspase inhibition reduces tubular apoptosis and proliferation and slows disease progression in polycystic Kidney disease.
- Pathways of caspase-mediated apoptosis in autosomal-dominant polycystic Kidney disease (ADPKD).
- Endotoxemic acute Renal failure is attenuated in caspase-1-deficient mice.
- Caspase-1-deficient mice are protected against cisplatin-induced apoptosis and acute tubular necrosis.
- Caspase inhibition prevents the increase in caspase-3, -2, -8 and -9 activity and apoptosis in the cold ischemic mouse Kidney.
- Urinary interleukin-18 is a marker of human acute tubular necrosis.
- Neutrophil-independent mechanisms of caspase-1- and IL-18-mediated ischemic acute tubular necrosis in mice.
Schools
Wayne State University School Of Medicine
Detroit Medical Center Program
University Of Colorado University Hospital Program
Procedures Preformed
- End-Stage Renal Disease Related Services
- Hemodialysis
Conditions Treated
- Acidosis
- Chronic Glomerulonephritis
- Chronic Kidney Diseases
- Congenital Cystic Kidney Disease
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Doctors Specialties
- Nephrology
Accepted Insurances
Education
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University of Colorado -
Wayne State University School of Medicine
Hospital
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University of Colorado Hospital
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1821188400 |
| Last Name Of The Provider | FAUBEL |
| First Name Of The Provider | SARAH |
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