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Barry J. Materson, MD, MBA

Arch Intern Med. 1996;156(3):239-240.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

FEW READERS of the ARCHIVES would be surprised by the statistic that about one third of all cases of end-stage renal disease are caused by diabetes mellitus. Yet, despite the advances in the treatment of diabetes that have evolved over more than half a century since insulin became available as a therapeutic agent, little progress had been made toward the protection of the kidneys as a target for diabetic microvascular disease. Very tight control of plasma glucose levels appears to offer protection, but at a cost of increased risk for hypoglycemic reactions.¹ The use of computer-based algorithms, insulin pumps, and islet cell transplantations may reduce the risk of tight control while retaining its benefits, but the cost will be high and not all diabetic patients will have access to these modalities.²

The demonstration by Lewis et al³ that the angiotensin-converting enzyme (ACE) inhibitor captopril could delay or . . . [Full Text PDF of this Article]

Author Affiliations
Department of Medicine University of Miami (M854) 1150 NW 14th St Miami, FL 33136

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