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Update of pathophysiology and management of diabetic kidney disease.
J Formos Med Assoc
August 2018
Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Diabetic kidney disease (DKD) is a major cause of morbidity and mortality in patients with diabetes mellitus and the leading cause of end-stage renal disease in the world. The most characteristic marker of DKD is albuminuria, which is associated with renal disease progression and cardiovascular events. Renal hemodynamics changes, oxidative stress, inflammation, hypoxia and overactive renin-angiotensin-aldosterone system (RAAS) are involved in the pathogenesis of DKD, and renal fibrosis plays the key role.
View Article and Find Full Text PDFEffect of ruboxistaurin on albuminuria and estimated GFR in people with diabetic peripheral neuropathy: results from a randomized trial.
Am J Kidney Dis
April 2015
Eli Lilly & Co, Indianapolis, Indiana. Electronic address:
Novel therapies of diabetic nephropathy.
Curr Opin Nephrol Hypertens
March 2009
Hypertensive Diseases Unit, Section of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Chicago, Pritzker School of Medicine, Chicago, Illinois 60637, USA.
Purpose Of Review: Current therapies proven to slow the progression of diabetic nephropathy include blockade of the renin-angiotensin system (RAS) with either angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Given our better understanding of the pathophysiology of diabetic nephropathy, newer therapies to treat this condition are slowly emerging.
Recent Findings: Animal studies and a single clinical trial demonstrate efficacy of the renin inhibitor, aliskiren, to decrease a marker of nephropathy progression, that is albuminuria.
Targeting the protein kinase C family in the diabetic kidney: lessons from analysis of mutant mice.
Diabetologia
May 2009
Department of Nephrology, Hannover Medical School, Hannover, Germany.
The protein kinase C (PKC) superfamily comprises proteins that are activated in response to various pathogenic stimuli in the diabetic state. Hyperglycaemia is the predominant stimulus that induces the activation of distinct PKC isoforms within a cell, each mediating specific functions, probably through differential subcellular localisation. The contribution of individual PKC isoforms can be directly addressed in vivo using innovative PKC-isoform-specific knockout (KO) mouse models, which are providing key insights into the physiological function of PKC isoform diversity in the development of diabetic nephropathy.
View Article and Find Full Text PDFEffect of protein kinase Cbeta inhibition on renal hemodynamic function and urinary biomarkers in humans with type 1 diabetes: a pilot study.
Diabetes Care
January 2009
Division of Medicine, University Health Network, Toronto, Canada.
Objective: The aim of this study was to examine the effect of protein kinase Cbeta inhibition with ruboxistaurin on renal hemodynamic function and urinary biomarkers (monocyte chemoattractant protein-1 [MCP-1] and epidermal growth factor) in renin angiotensin system blockade-treated type 1 diabetic subjects.
Research Design And Methods: Albuminuric subjects were randomized (2:1) to ruboxistaurin (32 mg daily; n = 13) or placebo (n = 7) for 8 weeks. Renal hemodynamic function was measured during clamped euglycemia or hyperglycemia and before and after ruboxistaurin or placebo.
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