Assistant Professor of Medicine and Pharmacology

Nephrology

James Luther is an expert in the field of Nephrology. He attended Vanderbilt University School of Medicine. James M. Luther has written publications. He has 35 publications published with PubMed. The lastest publication is: 'Treatment with Sildenafil Improves Insulin Sensitivity in Prediabetes: A Randomized, Controlled Trial.'

Publications

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• Aldosterone decreases glucose-stimulated insulin secretion in vivo in mice and in murine islets.
• Aldosterone deficiency and mineralocorticoid receptor antagonism prevent angiotensin II-induced cardiac, Renal, and vascular injury.
• Activation of the Endogenous Renin-Angiotensin-Aldosterone System or Aldosterone Administration Increases Urinary Exosomal Sodium Channel Excretion.
• Angiotensin II induces interleukin-6 in humans through a Mineralocorticoid receptor-dependent mechanism.
• Aldosterone in vascular and metabolic dysfunction.
• Treatment with Sildenafil Improves Insulin Sensitivity in Prediabetes: A Randomized, Controlled Trial.
• Human interventions to characterize novel relationships between the renin-angiotensin-aldosterone system and parathyroid hormone.
• Arg287Gln variant of EPHX2 and epoxyeicosatrienoic acids are associated with insulin sensitivity in humans.
• Effects of aldosterone on insulin sensitivity and secretion.
• Hypertension Is a Major Contributor to 20-Hydroxyeicosatetraenoic Acid-Mediated Kidney Injury in Diabetic Nephropathy.
• Is there a new dawn for selective Mineralocorticoid receptor antagonism?
• Aldosterone Deficiency prevents high-fat-feeding-induced hyperglycaemia and adipocyte dysfunction in mice.
• Fenofibrate lowers blood pressure in salt-sensitive but not salt-resistant Hypertension.
• Patient knowledge of blood pressure target is associated with improved blood pressure control in chronic Kidney disease.
• Sodium Intake, ACE Inhibition, and Progression to ESRD.
• Comparative Effects of Angiotensin-Converting Enzyme Inhibition and Angiotensin-Receptor Blockade on Inflammation during Hemodialysis.
• Proteomic analysis of urine exosomes by multidimensional protein identification technology (MudPIT).
• The renin-angiotensin-aldosterone system and glucose homeostasis.
• Inflammation and Hypertension: the interplay of interleukin-6, dietary sodium, and the renin-angiotensin system in humans.
• Aldosterone Postnatally, but not at Birth, Is Required for Optimal Induction of Renal Mineralocorticoid Receptor Expression and Sodium Reabsorption.
• Pharmacokinetics of acyclovir and its metabolites in cerebrospinal fluid and systemic circulation after administration of high-dose valacyclovir in subjects with norma...
• Endogenous bradykinin contributes to increased plasminogen activator inhibitor 1 antigen following hemodialysis.
• Endogenous aldosterone contributes to Acute angiotensin II-stimulated plasminogen activator inhibitor-1 and preproendothelin-1 expression in heart but not aorta.
• Aldosterone antagonism or synthase inhibition reduces end-organ damage induced by treatment with angiotensin and high salt.
• 'Labile hypertension' can be due to autonomic nervous system Failure.
• 17Beta-estradiol increases basal but not bradykinin-stimulated release of active t-PA in young postmenopausal women.
• Bradykinin type 2 receptor BE1 genotype influences bradykinin-dependent vasodilation during angiotensin-converting enzyme inhibition.
• Response to Interleukin-6 Antagonists for the Management of Hypertension.
• Bradykinin and its metabolite bradykinin 1-5 inhibit thrombin-induced platelet aggregation in humans.
• Angiotensin-converting enzyme inhibition increases basal vascular tissue plasminogen activator release in women but not in men.
• The bradykinin type 2 receptor BE1 polymorphism and ethnicity influence systolic blood pressure and vascular resistance.
• Blood pressure targets in hemodialysis patients.
• Protein profile of exosomes from trabecular meshwork cells.
• Utility of bone marrow biopsy for rapid diagnosis of febrile illnesses in patients with human immunoDeficiency virus infection.

Schools

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• Vanderbilt University

Conditions Treated

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• Acute Kidney Failure
• Calcium Metabolism Disorders
• Chronic Kidney Diseases
• Cryoglobulinemia
• View All

Doctors Specialties

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• Nephrology

Accepted Insurances

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Education

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• Vanderbilt University
• Vanderbilt University School of Medicine

Hospital

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• Vanderbilt Hospital and Clinics

Drug Facts

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NPI NUMBER		1295882165
NPPES Provider LastName		LUTHER
NPPES Provider FirstName		JAMES
NPPES Provider ZIPCode		372325356
NPPES Provider State		TN
Specialty Description		Nephrology
Total Claim Count		762.0
Distinct Opioid Count		0.0
Opioid Claim Count		0.0
Percent Opioid Claims		0.0

Helpful Reviews

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Medicare Facts

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National Provider Identifier [NPI]	1295882165
Last Name Of The Provider	LUTHER
First Name Of The Provider	JAMES
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