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Ronald T. Gansevoort, MD; Alfred J. Apperloo, MD; Jan E. Heeg, MD; Paul E. de Jong, MD; Dick de Zeeuw, MD
Groningen, the Netherlands

Arch Intern Med. 1992;152(10):2137-2138.

	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.—

In a recent article, Valentino and associates¹ present evidence that angiotensin-converting enzyme (ACE) inhibitors and certain calcium channel antagonists (CCAs) confer beneficial effects on renal function in diabetic nephropathy above and beyond those attributable solely to blood pressure lowering per se. In the same issue, Epstein,² in his editorial article, considers some of the issues raised by Valentino et al. Both articles^1,2 conclude, given the presently available data, that both ACE inhibitors and CCAs can effectively reduce urinary protein excretion and may preserve renal function. However, the effects of CCAs appear to vary considerably. Several factors are proposed by the authors that may explain the ultimate renal response to a CCA, including the type of CCA¹ and the level of preexisting renal function.² Although we tend to agree with the line of reasoning used by the authors of both articles, we would . . . [Full Text PDF of this Article]

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