C. Craig and Audrae Tisher Chair in Nephrology Professor of Medicine and Physiology and Functional Genomics University of Florida College of Medicine
Nephrology
Dr. I D. Weiner, MD
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Weiner is an expert in the field of Nephrology. He attended Vanderbilt University School of Medicine. He received 1 awards: "CMS Meaningful Use Stage 1 Certification". Weiner is a published doctor as well. He has 64 publications published. The latest was: H-K-ATPase in the RCCT-28A rabbit cortical collecting duct cell line. Doctor I D. Weiner, MD accepts all Medicare patients.
Publications
- NBCe1 expression is required for normal renal ammonia Metabolism.
- Effect of collecting duct-specific deletion of both Rh B Glycoprotein (Rhbg) and Rh C Glycoprotein (Rhcg) on renal response to metabolic Acidosis.
- Expression of glutamine synthetase in the mouse Kidney: localization in multiple epithelial cell types and differential regulation by hypokalemia.
- Expression of the ammonia transporter family member, Rh B Glycoprotein, in the human Kidney.
- Intercalated Cell-Specific Rh B Glycoprotein Deletion Diminishes Renal Ammonia Excretion Response to Hypokalemia.
- Renal Ammonia Excretion in Response to Hypokalemia: Effect of Collecting Duct-Specific Rh C Glycoprotein Deletion.
- Role of NH3 and NH4+ transporters in Renal acid-base transport.
- Role of the Rhesus glycoprotein, Rh B glycoprotein, in Renal ammonia excretion.
- Effect of intercalated cell-specific Rh C glycoprotein deletion on basal and metabolic Acidosis-stimulated renal ammonia excretion.
- Expression of ammonia transporter family members, Rh B glycoprotein and Rh C glycoprotein, in the developing rat Kidney.
- Expression of the gas-transporting proteins, Rh B glycoprotein and Rh C glycoprotein, in the murine lung.
- Collecting duct-specific Rh C glycoprotein deletion alters basal and Acidosis-stimulated renal ammonia excretion.
- Basolateral expression of the ammonia transporter family member Rh C glycoprotein in the mouse Kidney.
- Impaired acid secretion in cortical collecting duct intercalated cells from H-K-ATPase-deficient mice: role of HKalpha isoforms.
- Effects of ischemia-reperfusion injury on renal ammonia Metabolism and the collecting duct.
- Effect of reduced Renal mass on Renal ammonia transporter family, Rh C glycoprotein and Rh B glycoprotein, expression.
- Cellular distribution of the potassium channel KCNQ1 in normal mouse Kidney.
- Molecular mechanisms of Renal ammonia transport.
- Expression of the ammonia transporter, rh C glycoprotein, in normal and neoplastic human Kidney.
- Changes in subcellular distribution of the ammonia transporter, Rhcg, in response to chronic metabolic Acidosis.
- Renal expression of the ammonia transporters, Rhbg and Rhcg, in response to chronic metabolic Acidosis.
- Characterization of ammonia transport by the Kidney Rh glycoproteins RhBG and RhCG.
- Intercalated cell H+/OH- transporter expression is reduced in Slc26a4 null mice.
- Apical ammonia transport by the mouse inner medullary collecting duct cell (mIMCD-3).
- Expression of the ammonia transporter proteins Rh B glycoprotein and Rh C glycoprotein in the intestinal tract.
- Basolateral ammonium transport by the mouse inner medullary collecting duct cell (mIMCD-3).
- Localization of the ammonium transporters, Rh B glycoprotein and Rh C glycoprotein, in the mouse liver.
- Localization of the ammonium transporter proteins RhBG and RhCG in mouse Kidney.
- Renal microperfusion techniques.
- Expression and developmental regulation of the NMDA receptor subunits in the Kidney and cardiovascular system.
- Mechanisms through which ammonia regulates cortical collecting duct net proton secretion.
- Effects of ammonia on acid-base transport by the B-type intercalated cell.
- Effects of ammonia on bicarbonate transport in the cortical collecting duct.
- Apical proton secretion by the inner stripe of the outer medullary collecting duct.
- H-K-ATPase in the RCCT-28A rabbit cortical collecting duct cell line.
- Hyperkalemia: a potential silent killer.
- Regulation of B-type intercalated cell apical anion exchange activity by CO2/HCO3-.
- Intracellular pH regulation in the rabbit cortical collecting duct A-type intercalated cell.
- Hypokalemia--consequences, causes, and correction.
- H(+)-K(+)-ATPase in rabbit cortical collecting duct B-type intercalated cell.
- Optical studies of intracellular pH in Kidney cells in vitro.
- Regulation of luminal alkalinization and acidification in the cortical collecting duct by angiotensin II.
- Effect of hypokalemia on renal expression of the ammonia transporter family members, Rh B Glycoprotein and Rh C Glycoprotein, in the rat Kidney.
- Distribution of Cl-/HCO3- exchange and intercalated cells in rabbit cortical collecting duct.
- Mechanisms of bicarbonate transport by cultured rabbit inner medullary collecting duct cells.
- Regulation of intracellular pH in two cell populations of inner stripe of rabbit outer medullary collecting duct.
- Effect of epidermal growth factor on sodium transport in the cortical collecting tubule.
- Renal and hepatic expression of the ammonium transporter proteins, Rh B Glycoprotein and Rh C Glycoprotein.
- Use of fluorescent dye BCECF to measure intracellular pH in cortical collecting tubule.
- Expression of ammonia transporters, Rhbg and Rhcg, in Chronic cyclosporine nephropathy in rats.
- Renal ischemia-reperfusion injury causes intercalated cell-specific disruption of occludin in the collecting duct.
- Regulation of intracellular pH in the rabbit cortical collecting tubule.
- Molecular physiology of the Rh ammonia transport proteins.
- Expression of rh glycoproteins in the Mammalian Kidney.
- Regulation of Cl-/HCO3- exchange in the rabbit cortical collecting tubule.
- Angiotensin II acts through the angiotensin 1a receptor to upregulate pendrin.
- Structural-functional characteristics of acid-base transport in the rabbit collecting duct.
- The Rh gene family and Renal ammonium transport.
- Expression of the non-erythroid Rh glycoproteins in mammalian tissues.
- Primary hyperaldosteronism in a patient with end-stage renal Disease.
- Nocturia, aging, benign prostatic hypertrophy, and nocturnal vasopressin. A case report.
- A "weight-listing" paradox for candidates of Renal transplantation?
- Proximal tubule-specific glutamine synthetase deletion alters basal and Acidosis-stimulated ammonia metabolism.
Schools
Vanderbilt University School Of Medicine
University Tex Health Science Center
Procedures Preformed
- Hemodialysis
- Peritoneal Dialysis
Conditions Treated
- Acidosis
- Acute Kidney Failure
- Calcium Metabolism Disorders
- Chronic Kidney Diseases
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Doctors Specialties
- Nephrology
Accepted Insurances
- Aetna HMO
- Choice Plus POS II
- AvMed
- Blue Card PPO
- Blue Care HMO
- BlueDental Choice
- NetworkBlue
- Cigna HMO
- Cigna PPO
- Open Access Plus
- Employer Group PPO
- First Health (Coventry Health Care) PPO
- Choice Care PPO
- Select HMO
- Medicare MCR
- MultiPlan PPO
- PHCS Network PPO
- Choice Plus POS
- Navigate HMO
- Navigate POS
- Options PPO
- United Healthcare
Awards
- CMS Meaningful Use Stage 1 Certification
Education
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Washington University - Barnes-Jewish Hospital -
University of Texas Health Science Center -
Vanderbilt University School of Medicine
Hospital
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UF Health Shands Hospital
Drug Facts
| NPI NUMBER | 1790717155 | |
| NPPES Provider LastName | WEINER | |
| NPPES Provider FirstName | I | |
| NPPES Provider ZIPCode | 326103003 | |
| NPPES Provider State | FL | |
| Specialty Description | Nephrology | |
| Total Claim Count | 423.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1790717155 |
| Last Name Of The Provider | WEINER |
| First Name Of The Provider | I |
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