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John M. Poothullil, MD
Brazosport Memorial Hospital Lake Jackson, Tex

JAMA. 1995;273(10):773.

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

To the Editor.

—Dr Barbosa and colleagues¹ suggest a causal relationship between hyperglycemia and glomerular and vascular lesions that characterize the pathological findings in diabetic nephropathy.

Joslin² wrote that the chief cause of premature development of arteriosclerosis in diabetes was an excess of fat: an excess of fat in the body, an excess of fat in the diet, and an excess of fat in the blood. An editorial in JAMA reaffirmed this in 1989.³ Further, lack of correlation between a persistent hyperglycemic state and the development of diabetic nephropathy, neuropathy, and retinopathy has been demonstrated.⁴

Is it not possible that the lesser tendency to develop diabetic nephropathy in patients with better glycemic control resulted from favorable blood lipid and not glucose levels? Granted, both could result from good diabetic control. . . . [Full Text PDF of this Article]

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