T
Timothy W. Meyer
Researcher at Stanford University
Publications - 160
Citations - 11985
Timothy W. Meyer is an academic researcher from Stanford University. The author has contributed to research in topics: Renal function & Kidney. The author has an hindex of 52, co-authored 156 publications receiving 10946 citations. Previous affiliations of Timothy W. Meyer include Johns Hopkins University & Massachusetts Institute of Technology.
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Journal ArticleDOI
Dietary Protein Intake and the Progressive Nature of Kidney Disease: The Role of Hemodynamically Mediated Glomerular Injury in the Pathogenesis of Progressive Glomerular Sclerosis in Aging, Renal Ablation, and Intrinsic Renal Disease
TL;DR: With the development and increasingly widespread availability of dialysis and transplantation in the past three decades, relatively little attention has been paid to the influence of diet on the progression of renal disease, despite general awareness that renal disease typically follows an inexorably progressive course.
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Podocyte loss and progressive glomerular injury in type II diabetes.
Maria Enrica Pagtalunan,Peter L. Miller,Sara Jumping-Eagle,Sara Jumping-Eagle,Robert G. Nelson,Bryan D. Myers,Bryan D. Myers,Helmut G. Rennke,Norman S. Coplon,Norman S. Coplon,Limei Sun,Limei Sun,Timothy W. Meyer,Timothy W. Meyer +13 more
TL;DR: It is suggested that podocyte loss contributes to the progression of diabetic nephropathy.
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Predominance of hemodynamic rather than metabolic factors in the pathogenesis of diabetic glomerulopathy.
TL;DR: The findings indicate that the metabolic disorder seen in stable, moderately hyperglycemic diabetic rats does not lead to glomerulopathy as long as elevations in glomerular pressures and flows are prevented.
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Podocyte number predicts long-term urinary albumin excretion in Pima Indians with Type II diabetes and microalbuminuria.
TL;DR: It is suggested that podocytes play an important part in the development and progression of diabetic renal disease and neither mean arterial pressure nor HbA1 c changed substantially during follow-up.
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Angiotensin II receptor blockade limits glomerular injury in rats with reduced renal mass.
TL;DR: The results indicate that the effects of converting enzyme inhibition on remnant glomerular function and structure depend on reduction in AII activity and are not attributable simply to normalization of systemic blood pressure.