Professor, Medicine, University of Washington School of Medicine
Internal Medicine
Dr. Richard A. Zager, MD
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Richard Zager is an expert in the field of Internal Medicine. He attended Northwestern University Feinberg School of Medicine. Northwestern University Feinberg School of Medicine has a rank of 19 in research and a 29 in primary care Richard Zager is a published doctor and has 101 publications published. The lastest was: 'Use of high dose benzodiazepines in alcohol and sedative withdrawal delirium.'
Publications
- Marked protection against acute renal and hepatic injury after nitrited myoglobin + tin protoporphyrin administration.
- Acute hepatic ischemic-reperfusion injury induces a renal cortical "stress response," renal "cytoresistance," and an endotoxin hyperresponsive state.
- Renal Cortical Pyruvate Depletion during AKI.
- Progressive endothelin-1 gene activation initiates chronic/end-stage renal disease following experimental ischemic/reperfusion injury.
- Post-ischemic azotemia as a partial 'brake', slowing progressive kidney disease.
- Plasma and Urinary Heme Oxygenase-1 in Acute Kidney Injury.
- ACUTE UNILATERAL ISCHEMIC RENAL INJURY INDUCES PROGRESSIVE RENAL INFLAMMATION, LIPID ACCUMULATION,HISTONE MODIFICATION, AND 'END STAGE' KIDNEY DISEASE.
- HMG-CoA Reductase Activation and Urinary Pellet Cholesterol Elevations in Acute Kidney Injury.
- Renal cortical albumin gene induction and urinary albumin excretion in response to acute kidney injury.
- MCP-1 gene activation marks acute kidney injury.
- Acquired cytoresistance in the setting of hematopoietic cell transplantation.
- Parenteral iron formulations differentially affect MCP-1, HO-1, and NGAL gene expression and renal responses to injury.
- Progressive histone alterations and proinflammatory gene activation: consequences of heme protein/iron-mediated proximal tubule injury.
- Uremia impacts renal inflammatory cytokine gene expression in the setting of experimental acute kidney injury.
- BRG1 increases transcription of proinflammatory genes in renal ischemia.
- Renal ischemia-reperfusion injury upregulates histone-modifying enzyme systems and alters histone expression at proinflammatory/profibrotic genes.
- Uremia induces proximal tubular cytoresistance and heme oxygenase-1 expression in the absence of acute kidney injury.
- Renal ischemia-induced cholesterol loading: transcription factor recruitment and chromatin remodeling along the HMG CoA reductase gene.
- Growth and development alter susceptibility to acute renal injury.
- Endotoxin mediates recruitment of RNA polymerase II to target genes in acute renal failure.
- Maleate nephrotoxicity: mechanisms of injury and correlates with ischemic/hypoxic tubular cell death.
- Gentamicin suppresses endotoxin-driven TNF-alpha production in human and mouse proximal tubule cells.
- "Subclinical" gentamicin nephrotoxicity: a potential risk factor for exaggerated endotoxin-driven TNF-alpha production.
- Toll-like receptor (TLR4) shedding and depletion: acute proximal tubular cell responses to hypoxic and toxic injury.
- Acute renal failure: determinants and characteristics of the injury-induced hyperinflammatory response.
- Parenteral iron compounds: potent oxidants but mainstays of anemia management in chronic renal disease.
- Levosimendan protects against experimental endotoxemic acute renal failure.
- Intravenous iron therapy in peritoneal dialysis patients: short-term efficacy and long-term issues.
- IGF-1 induces rat glomerular mesangial cells to accumulate triglyceride.
- Parenteral iron treatment induces MCP-1 accumulation in plasma, normal kidneys, and in experimental nephropathy.
- Triglyceride accumulation in injured renal tubular cells: alterations in both synthetic and catabolic pathways.
- Parenteral iron compounds sensitize mice to injury-initiated TNF-alpha mRNA production and TNF-alpha release.
- Renal tubular triglyercide accumulation following endotoxic, toxic, and ischemic injury.
- Cholesterol synthesis and import contribute to protective cholesterol increments in acute myeloid leukemia cells.
- Parenteral iron nephrotoxicity: potential mechanisms and consequences.
- Parenteral iron therapy exacerbates experimental sepsis.
- Proximal tubular cytochrome c efflux: determinant, and potential marker, of mitochondrial injury.
- Adenovirus nephritis in hematopoietic stem-cell transplantation.
- Proximal tubular cholesterol loading after mitochondrial, but not glycolytic, blockade.
- Cytotoxicity of S-conjugates of the sevoflurane degradation product fluoromethyl-2,2-difluoro-1-(trifluoromethyl) vinyl ether (Compound A) in a human proximal tubular ...
- Radiographic contrast media-induced tubular injury: evaluation of oxidant stress and plasma membrane integrity.
- Acute tubular injury causes dysregulation of cellular cholesterol transport proteins.
- Cholesterol-modulating agents kill acute myeloid leukemia cells and sensitize them to therapeutics by blocking adaptive cholesterol responses.
- Sepsis syndrome stimulates proximal tubule cholesterol synthesis and suppresses the SR-B1 cholesterol transporter.
- Experimental glomerulopathy alters renal cortical cholesterol, SR-B1, ABCA1, and HMG CoA reductase expression.
- The mevalonate pathway during acute tubular injury: selected determinants and consequences.
- Parenteral iron formulations: a comparative toxicologic analysis and mechanisms of cell injury.
- Altered cholesterol localization and caveolin expression during the evolution of acute renal failure.
- Dephosphorylation of cell cycle-regulated proteins correlates with anoxia-induced suspended animation in Caenorhabditis elegans.
- Rapid renal alpha-1 antitrypsin gene induction in experimental and clinical acute kidney injury.
- Renal Cortical Lactate Dehydrogenase: A Useful, Accurate, Quantitative Marker of In Vivo Tubular Injury and Acute Renal Failure.
- Synchronous Recruitment of Epigenetic Modifiers to Endotoxin Synergistically Activated Tnf-α Gene in Acute Kidney Injury.
- Punch out the time clocks.
- Psychometrics of a neuropsychological test battery.
- Assessment of low-flow sevoflurane and isoflurane effects on renal function using sensitive markers of tubular toxicity.
- Use of high dose benzodiazepines in alcohol and sedative withdrawal delirium.
- Developmental well-being in offspring of women receiving cyclosporine post-renal transplant.
- Semiautomated enzymatic method for determining serum triglycerides by use of the Beckman "DSA 560".
- High dose daunorubicin (NSC-83142) in the treatment of advanced acute myelogenous leukemia.
- Funding for consultation-liaison services in public sector-managed care plans. The experience of the Consultation-Liaison Association of Philadelphia.
- Inorganic fluoride. Divergent effects on human proximal tubular cell viability.
- Pathogenetic mechanisms in nephrotoxic acute renal failure.
- Phospholipase A2: a potentially important determinant of adenosine triphosphate levels during hypoxic-reoxygenation tubular injury.
- Hemodialysis exacerbates enzymuria in patients with acute renal failure: brief report.
- Deferoxamine confers striking protection against cold storage injury to isolated mouse proximal tubules.
- Myoglobin inhibits proliferation of cultured human proximal tubular (HK-2) cells.
- Rhabdomyolysis and myohemoglobinuric acute renal failure.
- Phospholipase A2-induced cytoprotection of proximal tubules: potential determinants and specificity for ATP depletion-mediated injury.
- Marked enzymuria after bone marrow transplantation: a correlate of veno-occlusive disease-induced "hepatorenal syndrome".
- Mitochondrial free radical production induces lipid peroxidation during myohemoglobinuria.
- Iron, heme oxygenase, and glutathione: effects on myohemoglobinuric proximal tubular injury.
- Physiological pH. Effects on posthypoxic proximal tubular injury.
- Inorganic iron effects on in vitro hypoxic proximal renal tubular cell injury.
- Intracellular myoglobin loading worsens H2O2-induced, but not hypoxia/reoxygenation-induced, in vitro proximal tubular injury.
- Phospholipase A2 activity can protect renal tubules from oxygen deprivation injury.
- HK-2: an immortalized proximal tubule epithelial cell line from normal adult human kidney.
- Post-ischemic acute renal failure protects proximal tubules from O2 deprivation injury, possibly by inducing uremia.
- An evaluation of antioxidant effects on recovery from postischemic acute renal failure.
- An evaluation of renal tubular DNA laddering in response to oxygen deprivation and oxidant injury.
- Acute renal failure in the setting of bone marrow transplantation.
- Sepsis-associated acute renal failure: some potential pathogenetic and therapeutic insights.
- Postischemic proximal tubular resistance to oxidant stress and Ca2+ ionophore-induced attack. Implications for reperfusion injury.
- Obstruction of proximal tubules initiates cytoresistance against hypoxic damage.
- Heme protein-induced tubular cytoresistance: expression at the plasma membrane level.
- Protein synthesis inhibition induces cytoresistance in cultured human proximal tubular (HK-2) cells.
- Sphingosine: a mediator of acute renal tubular injury and subsequent cytoresistance.
- Rapid DNA fragmentation from hypoxia along the thick ascending limb of rat kidneys.
- Urinary protein markers of tubulointerstitial nephritis.
- Rapid radioimmunoassay for diagnosing acute tubular necrosis.
- Lysozyme and albumin radioimmunoassays. New techniques for the study of proteinuria.
- Effects of glucocorticoid administration on urinary albumin excretion by the normal kidney.
- A search for nephrotoxic factors within the uremic milieu.
- Susceptibility of the proximal tubular brush border to acute obstructive injury.
- Black urinary spherules and hyperphosphatemic renal failure.
- Gentamicin increases renal susceptibility to an acute ischemic insult.
- Mannitol interferes with the Du Pont aca method for inorganic phosphorus.
- Glomerulopathy does not increase renal susceptibility to acute ischemic injury.
- Progressive renal insufficiency induces increasing protection against ischemic acute renal failure.
- Potentiation of ischemic renal injury by amino acid infusion.
- Responses of the ischemic acute renal failure kidney to additional ischemic events.
Schools
Northwestern University The Feinberg School Of Medicine
Harbor Genl Hospital
UCLA Med Center
University Wash Med Center
Peter Bent Brigham Hospital
Doctors Specialties
- Nephrology
- Internal Medicine
Accepted Insurances
- Choice Plus POS II
- Blue Card PPO
- Cigna HMO
- Cigna PPO
- Great West Healthcare-Cigna PPO
- Open Access Plus
- First Choice Health PPO
- Coop Core
- ODS Health Plan
- Personal Option EPO
- Preferred Provider Network PPN
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Options PPO
Education
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Brigham and Women's Hospital -
Boston University Medical Center -
University of Washington -
UCLA Medical Center -
Harbor - UCLA Medical Center -
Northwestern University Feinberg School of Medicine
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