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There are two possible reasons for the discrepancy between Parving and colleagues' initial3 and most recent1 findings. Firstly, the controls in their first study were not matched to the cases for glycaemic control3 (unlike in our study2), yet diabetic nephropathy occurs only in patients with inadequate glycaemic control. Secondly, a deletion polymorphism of the angiotensin converting enzyme gene may act on the progression of, but not susceptibility to, diabetic nephropathy. In Parving and colleagues' latest study subjects homozygous
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