Schmidt S, Ritz E
Department of Internal Medicine/Renal Unit, Ruperto-Carola University of Heidelberg, Germany.
Curr Opin Nephrol Hypertens. 1996 Nov;5(6):552-5. doi: 10.1097/00041552-199611000-00016.
Some renal diseases (e.g. diabetic nephropathy and IgA glomerulonephritis) cluster within families, consistent with a strong genetic component for the development or progression of these diseases, or both. In this context it is attractive to examine the insertion/deletion polymorphism of the angiotensin I-converting enzyme. This polymorphism determines the concentration of angiotensin I-converting enzyme not only in serum, but also in tissues and thereby presumably the locally available concentration of angiotensin II. Several studies have examined whether this polymorphism is associated with the development of diabetic nephropathy, but most of these failed to show such an association. Studies in patients suffering from IgA glomerulonephritis or other renal diseases, including diabetic nephropathy, demonstrated that the insertion/ deletion polymorphism plays a role in the progression of renal diseases and in the response to treatment with angiotensin I-converting enzyme inhibitor.
一些肾脏疾病（如糖尿病肾病和IgA肾小球肾炎）在家族中聚集，这与这些疾病发生或进展中存在强大的遗传因素相符，或者两者皆有。在此背景下，研究血管紧张素I转换酶的插入/缺失多态性很有吸引力。这种多态性不仅决定血清中血管紧张素I转换酶的浓度，还决定组织中的浓度，因此推测也决定局部可用的血管紧张素II浓度。几项研究已检验这种多态性是否与糖尿病肾病的发生有关，但其中大多数未能显示出这种关联。对患有IgA肾小球肾炎或其他肾脏疾病（包括糖尿病肾病）的患者的研究表明，插入/缺失多态性在肾脏疾病进展以及对血管紧张素I转换酶抑制剂治疗的反应中起作用。
