Professor of Medicine, Baylor College of Medicine
Internal Medicine
Dr. William E. Mitch, MD
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William Mitch practices Internal Medicine. He attended Harvard Medical School. Harvard Medical School is a one of the best medicals schools. Harvard Medical School is ranked 1/12 in Research/PrimaryCare. He has 4 awards "CMS Meaningful Use Stage 1 Certification", "Elected Member", "Whos Who in Medicine and Healthcare" and "Fellow (ASNF)". William Mitch is a published MD. He published 71 publications, including: 'CKD Stimulates Muscle Protein Loss Via Rho-associated Protein Kinase 1 Activation.' He is registered with Medicare and accepts Medicare payments.
Publications
- Migration of smooth muscle cells from the arterial anastomosis of arteriovenous fistulas requires Notch activation to form neointima.
- Protective Role of Insulin-Like Growth Factor-1 Receptor in Endothelial Cells against Unilateral Ureteral Obstruction-Induced Renal Fibrosis.
- Low-protein diets in Chronic kidney disease: are we finally reaching a consensus?
- Can Muscle-Kidney Crosstalk Slow Progression of CKD?
- Mechanisms of muscle wasting in Chronic kidney disease.
- MicroRNA-29 induces cellular senescence in aging muscle through multiple signaling pathways.
- Blocking Notch in Endothelial Cells Prevents Arteriovenous Fistula Failure Despite CKD.
- Molecular mechanisms and signaling pathways of angiotensin II-induced muscle wasting: Potential therapeutic targets for cardiac cachexia.
- Myostatin/activin pathway antagonism: Molecular basis and therapeutic potential.
- Stat3 Activation Links a C/EBPδ to Myostatin Pathway to Stimulate Loss of Muscle Mass.
- Muscle wasting from Kidney failure-A model for catabolic conditions.
- Signal regulatory protein-? interacts with the insulin receptor contributing to muscle wasting in Chronic kidney disease.
- The mean dietary protein intake at different stages of Chronic kidney disease is higher than current guidelines.
- Mechanisms stimulating muscle wasting in Chronic kidney disease: the roles of the ubiquitin-proteasome system and myostatin.
- Loss of Glutathione S-transferase A4 Accelerates Obstruction-induced Tubule Damage and Renal Fibrosis.
- Targeting the myostatin signaling pathway to treat muscle wasting Diseases.
- Requirement of argininosuccinate lyase for systemic nitric oxide production.
- Decreased miR-29 Suppresses Myogenesis in CKD.
- Angiotensin II Upregulates Protein Phosphatase 2C{alpha} and Inhibits AMP-Activated Protein Kinase Signaling and Energy Balance Leading to Skeletal Muscle Wasting.
- OPPORTUNITYTM: a large-scale randomized clinical trial of growth hormone in hemodialysis patients.
- Proteins and Renal fibrosis: low-protein diets induce Kruppel-like factor-15, limiting Renal fibrosis.
- Pharmacological inhibition of myostatin suppresses systemic inflammation and muscle atrophy in mice with Chronic kidney disease.
- Proteolysis by the ubiquitin-proteasome system and Kidney disease.
- Caspase-3 cleaves specific 19 S proteasome subunits in skeletal muscle stimulating proteasome activity.
- PTEN inhibition improves muscle regeneration in mice fed a high-fat diet.
- Review of muscle wasting associated with Chronic kidney disease.
- Satellite cell dysfunction and impaired IGF-1 signaling cause CKD-induced muscle atrophy.
- Chemokine CXCL16 regulates neutrophil and macrophage infiltration into injured muscle, promoting muscle regeneration.
- Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice.
- Exercise ameliorates chronic kidney disease-induced defects in muscle protein Metabolism and progenitor cell function.
- IL-6 and serum amyloid A synergy mediates angiotensin II-induced muscle wasting.
- Influence of renal function and diet on acid-base status in Chronic kidney disease patients.
- Navigating between the Scylla and Charybdis of prescribing dietary protein for Chronic kidney diseases.
- OPPORTUNITY: a randomized clinical trial of growth hormone on outcome in hemodialysis patients.
- Ghrelin treatment of Chronic kidney disease: improvements in lean body mass and cytokine profile.
- PTEN expression contributes to the regulation of muscle protein degradation in Diabetes.
- Tissue-specific regulation of ubiquitin (UbC) transcription by glucocorticoids: in vivo and in vitro analyses.
- Malnutrition is an unusual cause of decreased muscle mass in Chronic kidney disease.
- Development of a diagnostic method for detecting increased muscle protein degradation in patients With catabolic conditions.
- Insulin resistance accelerates muscle protein degradation: Activation of the ubiquitin-proteasome pathway by defects in muscle cell signaling.
- Effect of bicarbonate on muscle protein in patients receiving hemodialysis.
- Proteolytic mechanisms, not malnutrition, cause loss of muscle mass in Kidney failure.
- Protein degradation by the ubiquitin-proteasome pathway in normal and Disease states.
- Chronic kidney disease causes defects in signaling through the insulin receptor substrate/phosphatidylinositol 3-kinase/Akt pathway: implications for muscle atrophy.
- Cachexia in Chronic kidney disease: a link to defective central nervous system control of appetite.
- Beneficial responses to modified diets in treating patients with Chronic kidney disease.
- 2004 Presidential Address: An evaluation of progress toward goals.
- Muscle-specific expression of IGF-1 blocks angiotensin II-induced skeletal muscle wasting.
- Strategies for suppressing muscle atrophy in Chronic kidney disease: mechanisms activating distinct proteolytic systems.
- Treating diabetic Nephropathy--are there only economic issues?
- Detecting and managing patients with type 2 diabetic Kidney disease: proteinuria and cardiovascular disease.
- The evidence against malnutrition as a prominent problem for Chronic dialysis patients.
- Cellular mechanisms causing loss of muscle mass in Kidney disease.
- Albuminuria, a therapeutic target for cardiovascular protection in type 2 diabetic patients With nephropathy.
- Proteinuria, a target for renoprotection in patients With type 2 diabetic nephropathy: lessons from RENAAL.
- Regulation of muscle protein degradation: coordinated control of apoptotic and ubiquitin-proteasome systems by phosphatidylinositol 3 kinase.
- Activation of caspase-3 is an initial step triggering accelerated muscle proteolysis in catabolic conditions.
- Diets for patients with Chronic kidney disease, still worth prescribing.
- Multiple types of skeletal muscle atrophy involve a common program of changes in gene expression.
- Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in Hypertension.
- Mechanisms activating proteolysis to cause muscle atrophy in catabolic conditions.
- Getting beyond cross-sectional studies of abnormal nutritional indexes in dialysis patients.
- The precision of estimating protein intake of patients with Chronic renal failure.
- Malnutrition: a frequent misdiagnosis for hemodialysis patients.
- Relationships among inflammation nutrition and physiologic mechanisms establishing albumin levels in hemodialysis patients.
- Ubiquitin (UbC) expression in muscle cells is increased by glucocorticoids through a mechanism involving Sp1 and MEK1.
- Prevention Conference VI: Diabetes and Cardiovascular Disease: Writing Group V: management of cardiovascular-renal complications.
- Nutrition in CAPD: serum bicarbonate and the ubiquitin-proteasome system in muscle.
- Insights into the abnormalities of Chronic renal disease attributed to malnutrition.
- CKD Stimulates Muscle Protein Loss Via Rho-associated Protein Kinase 1 Activation.
Schools
Harvard Medical School
Peter Bent Brigham Hospital
Brigham Womens Hospital
Nci
Johns Hopkins Hospital
Procedures Preformed
- Hemodialysis
- Peritoneal Dialysis
Conditions Treated
- Acidosis
- Calcium Metabolism Disorders
- Chronic Kidney Diseases
- Diabetes With Renal Manifestations
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Doctors Specialties
- Nephrology
- Internal Medicine
Accepted Insurances
Awards
- CMS Meaningful Use Stage 1 Certification
- Elected Member
- Whos Who in Medicine and Healthcare
- Fellow (ASNF)
Education
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Brigham and Women's Hospital -
Johns Hopkins University -
Harvard Medical School
Hospital
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Michael E. DeBakey Veterans Affairs Medical Center -
Harris Health System -
Texas Children's Hospital
Drug Facts
| NPI NUMBER | 1013001288 | |
| NPPES Provider LastName | MITCH | |
| NPPES Provider FirstName | WILLIAM | |
| NPPES Provider ZIPCode | 770303411 | |
| NPPES Provider State | TX | |
| Specialty Description | Nephrology | |
| Total Claim Count | 279.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1013001288 |
| Last Name Of The Provider | MITCH |
| First Name Of The Provider | WILLIAM |
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