Packer M, Lee W H, Medina N, Yushak M, Kessler P D
Ann Intern Med. 1987 Mar;106(3):346-54. doi: 10.7326/0003-4819-106-3-346.
Renal function was evaluated in 104 patients with severe chronic heart failure whom we treated with captopril or enalapril. Seventy patients showed no change or an improvement in renal function (group A), and 34 patients developed functional renal insufficiency (group B). Before converting-enzyme inhibition, group B patients received higher doses of furosemide (p less than 0.02) and had lower central venous pressures (p less than 0.05) than group A patients. After 1 to 3 months of converting-enzyme inhibition, an excessive reduction in left ventricular filling pressure (to less than 15 mm Hg) or mean arterial pressure (to less than 60 mm Hg) was noted in 28 of 34 (82%) patients in group B but in only 22 of 70 patients in group A (31%) (p less than 0.001). At the end of the study, drug-induced azotemia resolved after a reduction in the dosage of diuretics, despite unaltered treatment with captopril and enalapril. Hence, the deterioration of renal function after converting-enzyme inhibition in heart failure is not a toxic or immunologic reaction to therapy but results from specific hemodynamic events that can be ameliorated by sodium repletion.
我们用卡托普利或依那普利治疗了104例重度慢性心力衰竭患者,并对其肾功能进行了评估。70例患者肾功能无变化或有所改善(A组),34例患者出现功能性肾功能不全(B组)。在进行转换酶抑制治疗前,B组患者服用的速尿剂量高于A组患者(p<0.02),中心静脉压低于A组患者(p<0.05)。在进行1至3个月的转换酶抑制治疗后,B组34例患者中有28例(82%)出现左心室充盈压过度降低(降至低于15 mmHg)或平均动脉压过度降低(降至低于60 mmHg),而A组70例患者中只有22例(31%)出现这种情况(p<0.001)。在研究结束时,尽管卡托普利和依那普利的治疗未改变,但在减少利尿剂剂量后,药物性氮质血症得到缓解。因此,心力衰竭患者在进行转换酶抑制治疗后肾功能恶化并非对治疗的毒性或免疫反应,而是由特定的血流动力学事件导致的,补充钠可改善这些事件。