Eisenhauer T, Jungmann E, Warneboldt D, Ansorge G, Scherberich J, Talartschik J
Abteilung Nephrologie und Rheumatologie des Zentrums Innere Medizin, Universitätsklinik Göttingen.
Klin Wochenschr. 1990 Aug 2;68(15):750-7. doi: 10.1007/BF01647243.
Renal functional reserve capacity was evaluated in 19 normotensive type I diabetics without microalbuminuria. All patients had normal basal renal function as assessed by 24-hour creatinine clearances higher than 120 ml/min. PAH, inulin, and creatinine clearances were carried out every hour before, during, and after infusion of an amino acid (AA) solution. The same experiment was repeated after ACE inhibition with captopril (25 mg). Two groups of patients were found: Group A (responders) showed a significant rise in GFR after AA infusion (inulin clearances from 117 +/- 8 to 138 +/- 10 ml/min) (p less than 0.05), whereas in Group B (non-responders) no significant change in GFR was observed. Groups were comparable in age, duration of diabetes, metabolic control, and mean arterial blood pressure. Group B, however, had a significantly higher basal inulin clearance (167 +/- 17 ml/min) than Group A (117 +/- 8 ml/min). In Group A ACE inhibition completely blocked the AA-induced rise in GFR, while basal GFR in Group B was significantly reduced (167 +/- 17 to 148 +/- 8 ml/min) after captopril administration. In both groups renal plasma flow was enhanced by ACE inhibition. A rise in glucagon was observed in all patients during AA infusion. It is concluded that type I diabetics with normal basal renal function already have reduced (Group A) renal functional reserve capacity, which is completely abolished (Group B) when concomitant hyperfiltration occurs. ACE inhibition reduces hyperfiltration and is capable of blocking the AA-induced rise in GFR in these patients.
对19例无微量白蛋白尿的血压正常的I型糖尿病患者的肾功能储备能力进行了评估。所有患者的基础肾功能均正常，24小时肌酐清除率高于120 ml/min。在输注氨基酸（AA）溶液之前、期间和之后，每小时进行一次对氨基马尿酸（PAH）、菊粉和肌酐清除率测定。在用卡托普利（25 mg）进行血管紧张素转换酶（ACE）抑制后，重复相同实验。发现两组患者：A组（反应者）在输注AA后肾小球滤过率（GFR）显著升高（菊粉清除率从117±8 ml/min升至138±10 ml/min）（p<0.05），而B组（无反应者）未观察到GFR有显著变化。两组在年龄、糖尿病病程、代谢控制和平均动脉血压方面具有可比性。然而，B组的基础菊粉清除率（167±17 ml/min）显著高于A组（117±8 ml/min）。在A组中，ACE抑制完全阻断了AA诱导的GFR升高，而在B组中，给予卡托普利后基础GFR显著降低（从167±17 ml/min降至148±8 ml/min）。在两组中，ACE抑制均增强了肾血浆流量。在输注AA期间，所有患者均观察到胰高血糖素升高。结论是，基础肾功能正常的I型糖尿病患者已经存在肾功能储备能力降低（A组），当伴有超滤过发生时，这种能力会完全丧失（B组）。ACE抑制可减少超滤过，并能够阻断这些患者中AA诱导的GFR升高。
