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

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ACE insertion/deletion (I/D) polymorphism and diabetic nephropathy.

Zohreh Rahimi¹

¹Medical Biology Research Center and Department of Biochemistry, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Journal of Nephropathology

|January 30, 2014

Summary

The Angiotensin Converting Enzyme (ACE) insertion/deletion (I/D) polymorphism influences ACE levels, with the DD genotype showing higher activity. This genetic variation is crucial for understanding diabetic nephropathy risk and treatment responses.

Keywords:

ACE I/D polymorphism ACE activity ACE inhibitors Angiotensin II receptor blockers Diabetic nephropathy

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Area of Science:

Genetics
Cardiovascular Physiology
Nephrology

Background:

The renin-angiotensin system (RAS) regulates blood pressure via Angiotensin Converting Enzyme (ACE).
ACE gene variations, specifically the I/D polymorphism, impact ACE activity and angiotensin II levels.

Purpose of the Study:

To review the influence of ACE I/D polymorphism on diabetic nephropathy.
To examine the association between ACE I/D polymorphism and responses to RAS-targeting therapies.
To discuss gene-environment interactions in diabetic nephropathy development.

Main Methods:

Comprehensive literature search of major scientific databases (DOAJ, Google Scholar, PubMed, LISTA, Web of Science).
Review and synthesis of existing studies on ACE I/D polymorphism and diabetic nephropathy.

Main Results:

The ACE I/D polymorphism significantly affects plasma ACE levels.
The DD genotype is linked to higher systemic and renal ACE levels compared to the II genotype.

Conclusions:

ACE I/D polymorphism is a key factor in diabetic nephropathy onset and progression.
Understanding this polymorphism aids in predicting patient response to ACE inhibitors and angiotensin II receptor antagonists.
Further research into synergistic genetic effects is warranted for a comprehensive risk assessment.