Hannedouche T, Natov S, Garev L, Marquez L P, Delgado A, Boitard C, Lacour B, Grünfeld J P
Département de Néphrologie, Hôpital Necker, Paris, France.
Nephrol Dial Transplant. 1990;5(3):168-73. doi: 10.1093/ndt/5.3.168.
To investigate the time relationships involved in cyclosporin-induced nephrotoxicity we studied changes in blood pressure, renal haemodynamics and sodium excretion in 22 adult patients with insulin-dependent diabetes mellitus treated with cyclosporin (CsA) for 4 +/- 2 days, compared to 22 insulin-dependent diabetic patients receiving conventional insulin therapy, who were matched for age and duration of diabetes. To further clarify the pathogenic role of the renin-angiotensin system, insulin-dependent diabetic patients receiving CsA were studied before and after sublingual administration of 75 mg captopril. An average of 4 days CsA treatment markedly increased blood pressure and renal vascular resistance, but did not alter glomerular filtration rate, renal plasma flow, sodium urinary excretion, or body-weight. The marked renal vasoconstriction without early changes in GFR suggests that the late decrease in GFR may involve other factors in addition to renal hypoperfusion. Acute inhibition of angiotension II formation was still able to decrease blood pressure and renal vascular resistance, although not to normal control values. These results indicate that a physiological concentration of angiotensin II may potentialise but may not be the sole factor involved in the vasopressor effect of CsA.
为了研究环孢素诱导肾毒性所涉及的时间关系，我们对22例接受环孢素（CsA）治疗4±2天的成年胰岛素依赖型糖尿病患者的血压、肾血流动力学和钠排泄变化进行了研究，并与22例接受常规胰岛素治疗、年龄和糖尿病病程相匹配的胰岛素依赖型糖尿病患者进行了比较。为了进一步阐明肾素-血管紧张素系统的致病作用，我们对接受CsA治疗的胰岛素依赖型糖尿病患者在舌下含服75毫克卡托普利前后进行了研究。平均4天的CsA治疗显著升高了血压和肾血管阻力，但未改变肾小球滤过率、肾血浆流量、尿钠排泄或体重。明显的肾血管收缩而GFR无早期变化表明，GFR的后期下降可能除了肾灌注不足外还涉及其他因素。急性抑制血管紧张素II的形成仍能降低血压和肾血管阻力，尽管未降至正常对照值。这些结果表明，生理浓度的血管紧张素II可能会增强，但可能不是CsA升压作用的唯一因素。
