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Diabetic Nephropathy

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Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration...

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Related Experiment Video

Updated: May 1, 2026

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

Published on: May 2, 2025

Renal endothelial dysfunction in diabetic nephropathy.

Huifang Cheng, Raymond C Harris¹

¹Division of Nephrology, S3223 MCN, Vanderbilt University School of Medicine, and Nashville Veterans Affairs Hospital, Nashville, TN 37232, USA. huifang.cheng@vanderbilt.edu.

Cardiovascular & Hematological Disorders Drug Targets

|April 12, 2014

Summary

This summary is machine-generated.

Diabetic nephropathy (DN) involves endothelial dysfunction, impacting kidney microcirculation. Strategies targeting endothelial nitric oxide synthase (eNOS) and promoting cell regeneration offer hope for DN treatment.

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Last Updated: May 1, 2026

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

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Published on: May 2, 2025

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Published on: October 15, 2010

Area of Science:

Nephrology
Vascular Biology
Diabetology

Background:

Endothelial dysfunction is a key factor in diabetic nephropathy (DN) pathogenesis.
Heterogeneity of endothelial cells (ECs) complicates understanding diabetic stimuli responses.
Direct in vivo measurement of EC function is limited, relying on indirect markers of EC injury.

Purpose of the Study:

To explore the role of endothelial dysfunction in diabetic nephropathy.
To investigate the mechanisms of endothelial cell injury in the kidney microcirculation.
To identify potential therapeutic targets for restoring endothelial function in DN.

Main Methods:

Review of current literature on endothelial dysfunction in DN.
Analysis of the role of hyperglycemia and metabolic consequences in EC dysfunction.
Examination of endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) bioavailability.

Main Results:

Hyperglycemia and metabolic dysregulation contribute to EC dysfunction in DN.
Impaired eNOS activity (uncoupling, modifications, decreased expression) reduces NO bioavailability.
Reduced NO bioavailability exacerbates oxidative stress, promoting further EC injury and inflammation.

Conclusions:

Injured ECs act as signal transducers, initiating inflammatory and profibrotic responses in DN.
Pharmacological and regenerative therapies show promise for restoring EC function in diabetic nephropathy.