Professor of Medicine
Nephrology
Dr. Wilfred Lieberthal, MD
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Wilfred Lieberthal works in the field of Nephrology. Dr. Wilfred Lieberthal is a published doctor and has 77 publications published. The lastest was: 'Role of superoxide in apoptosis induced by growth factor withdrawal.' Dr. Wilfred Lieberthal accepts all Medicare patients.
Publications
- Rapamycin impairs recovery from Acute renal failure: role of cell-cycle arrest and apoptosis of tubular cells.
- Anemia-induced increase in the bleeding time: implications for treatment of nonsurgical blood loss.
- Role of apoptosis of renal tubular cells in Acute renal failure: therapeutic implications.
- Acute renal failure. III. The role of growth factors in the process of renal regeneration and repair.
- Mouse proximal tubular cell-cell adhesion inhibits apoptosis by a cadherin-dependent mechanism.
- Acute renal failure. II. Experimental models of Acute renal failure: imperfect but indispensable.
- Effects of hemoglobin-based oxygen-carrying solutions in anesthetized rats with Acute ischemic renal failure.
- Albumin is a major serum survival factor for Renal tubular cells and macrophages through scavenging of ROS.
- ATP depletion increases tyrosine phosphorylation of beta-catenin and plakoglobin in Renal tubular cells.
- Plasmalogens as endogenous antioxidants: somatic cell mutants reveal the importance of the vinyl ether.
- O-raffinose cross-linking markedly reduces systemic and Renal vasoconstrictor effects of unmodified human hemoglobin.
- Role of superoxide in apoptosis induced by growth factor Withdrawal.
- Acute renal failure. I. Relative importance of proximal vs. distal tubular injury.
- Necrosis and apoptosis in Acute renal failure.
- Lysophosphatidic acid is a major serum noncytokine survival factor for murine macrophages which acts via the phosphatidylinositol 3-kinase signaling pathway.
- Biology of ischemic and toxic Renal tubular cell injury: role of nitric oxide and the inflammatory response.
- Graded ATP depletion can cause necrosis or apoptosis of cultured mouse proximal tubular cells.
- Lysophosphatidic acid: a novel growth and survival factor for Renal proximal tubular cells.
- Heat stress ameliorates ATP depletion-induced sublethal injury in mouse proximal tubule cells.
- Beta1 integrin-mediated adhesion between Renal tubular cells after anoxic injury.
- Fatty acid-induced cytotoxicity: differences in susceptibility between MDCK cells and primary cultures of proximal tubular cells.
- Effects of nitric oxide inhibition on systemic and Renal hemodynamics in the hemorrhaged rat.
- Mechanisms of death induced by cisplatin in proximal tubular epithelial cells: apoptosis vs. necrosis.
- Mechanisms of apoptosis and its potential role in Renal tubular epithelial cell injury.
- Lipid peroxidation contributes to hydrogen peroxide induced cytotoxicity in Renal epithelial cells.
- Anti-phospholipid autoantibodies bind to apoptotic, but not viable, thymocytes in a beta 2-glycoprotein I-dependent manner.
- Integrin receptors in renal tubular epithelium: new insights into pathophysiology of Acute renal failure.
- Functional and cytoskeletal changes induced by sublethal injury in proximal tubular epithelial cells.
- Renal mouse proximal tubular cells are more susceptible than MDCK cells to chemical anoxia.
- Stroma-free hemoglobin increases blood pressure and GFR in the hypotensive rat: role of nitric oxide.
- Clinical relevance of the natriuretic peptides in edematous states.
- Stroma-free hemoglobin: a potential blood substitute.
- Endothelin receptor A blockade alters hemodynamic response to nitric oxide inhibition in rats.
- The effect of cations on the activity of human urinary kallikrein.
- Antibody that recognizes total human urinary kallikrein: radioimmunological determination of inactive kallikrein.
- Effects of alterations in sodium and water Metabolism on urinary excretion of active and inactive kallikrein in man.
- Reduced ratio of active-to-total urinary kallikrein in essential Hypertension.
- Control of rat Renal vascular resistance during alterations in sodium balance.
- Stimulation of prostaGlandin production in rat glomerular epithelial cells by antidiuretic hormone.
- Interactions between ADH and prostaglandins in isolated erythrocyte-perfused rat Kidney.
- Effect of erythrocytes on the function and morphology of the isolated perfused rat Kidney.
- Hemodynamic effects of different preparations of stroma free hemolysates in the isolated perfused rat Kidney.
- Ischemia in the isolated erythrocyte-perfused rat Kidney. Protective effect of hypothermia.
- Vasopressin stimulates urinary kallikrein excretion in the isolated erythrocyte-perfused rat Kidney.
- Effects of stroma-free hemoglobin solutions on isolated perfused rabbit hearts and isolated perfused rat Kidneys.
- A role for thromboxane in complement-mediated glomerular injury.
- Renal ischemia and reperfusion impair endothelium-dependent vascular relaxation.
- Studies of the mechanism of the vasoconstrictor activity of stroma-free hemoglobin in the isolated perfused rat Kidney and rabbit heart.
- Cytosolic Calcium and protein kinase C reduce complement-mediated glomerular epithelial injury.
- Protective effect of atrial natriuretic factor and mannitol following Renal ischemia.
- Treatment of Acute tubular necrosis.
- Nitric oxide inhibition in rats improves blood pressure and Renal function during hypovolemic shock.
- Effects of atrial natriuretic factor in ischemic renal injury: studies in the isolated erythrocyte-perfused rat Kidney.
- 19-nor-DOC biosynthesis in the isolated perfused rat Kidney.
- Role of thromboxane in mediating the intrarenal vasoconstriction induced by unmodified stroma free hemoglobin in the isolated perfused rat Kidney.
- Rapid recurrence of membranous Nephropathy in a related allograft.
- AMPK protects proximal tubular cells from stress-induced apoptosis by an ATP-independent mechanism: potential role of Akt activation.
- Recognition of apoptotic cells by epithelial cells: conserved versus tissue-specific signaling responses.
- The role of the mammalian target of rapamycin (mTOR) in Renal disease.
- Apoptotic and necrotic cells as sentinels of local tissue stress and inflammation: response pathways initiated in nearby viable cells.
- Macroautophagy: a mechanism for mediating cell death or for promoting cell survival?
- Rapamycin delays but does not prevent recovery from Acute renal failure: role of acquired tubular resistance.
- A comparison of the Acute hemodynamic and delayed effects of 50% exchange transfusion with two different cross-linked hemoglobin based oxygen carrying solutions and Pe...
- Primary prevention of Acute renal failure in the critically ill.
- Risk factors for Acute renal failure: inherent and modifiable risks.
- Rapamycin ameliorates proteinuria-associated tubulointerstitial inflammation and fibrosis in experimental membranous Nephropathy.
- Lithium activates the Wnt and phosphatidylinositol 3-kinase Akt signaling pathways to promote cell survival in the absence of soluble survival factors.
- Inhibition of ligand-independent ERK1/2 activity in Kidney proximal tubular cells deprived of soluble survival factors up-regulates Akt and prevents apoptosis.
- Quantitative assessment of tyrosine nitration of manganese superoxide dismutase in angiotensin II-infused rat Kidney.
- Animal models of Acute tubular necrosis.
- Chemical anoxia of tubular cells induces activation of c-Src and its translocation to the zonula adherens.
- Phagocytosis of apoptotic cells by macrophages induces novel signaling events leading to cytokine-independent survival and inhibition of proliferation: activation of A...
- Acute renal failure in the critically ill patient.
- Role of apoptosis in the pathogenesis of Acute renal failure.
- ATP depletion of tubular cells causes dissociation of the zonula adherens and nuclear translocation of beta-catenin and LEF-1.
- Comparison of the effects of a 50% exchange-transfusion With albumin, hetastarch, and modified hemoglobin solutions.
Schools
University Of The Witwatersrand Faculty Of Health Sciences
Procedures Preformed
- Arteriovenostomy for Renal Dialysis
- Hemodialysis
- Peritoneal Dialysis
Conditions Treated
- Acidosis
- Acute Glomerulonephritis
- Acute Kidney Failure
- Calcium Metabolism Disorders
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Doctors Specialties
- Nephrology
Accepted Insurances
- Aetna HMO
- Choice Plus POS II
- Amerigroup (Wellpoint)
- Blue Card PPO
- Cigna HMO
- Cigna PPO
- Great West Healthcare-Cigna PPO
- Open Access Plus
- Commercial Insurance Company
- CoreSource
- Emblem Health
- GHI PPO
- Health Insurance Plan of Greater New York (HIP) PPO
- Fidelis Care HMO
- HealthFirst
- Choice Care PPO
- Medicaid
- Medicare MCR
- MultiPlan PPO
- PHCS Network PPO
- National Elevator
- Neighborhood Health Plan
- Freedom Plan
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Options PPO
- Oxford Liberty
- United Healthcare
Education
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Boston University Medical Center -
University of the Witwatersrand
Hospital
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Stony Brook University Medical Center
Drug Facts
| NPI NUMBER | 1972518793 | |
| NPPES Provider LastName | LIEBERTHAL | |
| NPPES Provider FirstName | WILFRED | |
| NPPES Provider ZIPCode | 11733 | |
| NPPES Provider State | NY | |
| Specialty Description | Nephrology | |
| Total Claim Count | 12.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1972518793 |
| Last Name Of The Provider | LIEBERTHAL |
| First Name Of The Provider | WILFRED |
| View All |
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