Appropriate drug therapy for improving outcomes in diabetic nephropathy.

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Diabetic nephropathy is the leading cause of end-stage kidney disease in the United States. The majority of these cases are attributed to those with type 2 diabetes. Elevated blood pressure, proteinuria, and increased activity of the renin-angiotensin-aldosterone system (RAAS) play a major role in the development and progression of chronic kidney disease attributed to diabetes mellitus. Moreover, drugs that inhibit angiotensin II synthesis or block the angiotensin II type I receptor lower blood pressure, reduce proteinuria, and improve outcomes in patients with chronic kidney disease caused by diabetes. This article highlights improvements in the current management of diabetic nephropathy afforded by agents that inhibit the RAAS, discusses their limitations, and considers novel strategies to prevent onset and progression of diabetic nephropathy. Current opinions concerning combination drug therapy with agents that block the RAAS at multiple sites, as well as combining calcium channel blockers with either angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists, are also discussed.

Original languageEnglish (US)
Pages (from-to)545-552
Number of pages8
JournalCurr Diab Rep
Volume2
Issue number6
StatePublished - Dec 2002

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Diabetic Nephropathies
Renin-Angiotensin System
Chronic Renal Insufficiency
Proteinuria
Drug Therapy
Blood Pressure
Angiotensin I
Angiotensin Receptors
Angiotensin Receptor Antagonists
Calcium Channel Blockers
Combination Drug Therapy
Angiotensin-Converting Enzyme Inhibitors
Angiotensin II
Type 2 Diabetes Mellitus
Chronic Kidney Failure
Diabetes Mellitus
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Cardiology and Cardiovascular Medicine

Cite this

Appropriate drug therapy for improving outcomes in diabetic nephropathy. / Toto, Robert D.

In: Curr Diab Rep, Vol. 2, No. 6, 12.2002, p. 545-552.

Research output: Contribution to journalArticle

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