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低GFR患者代谢性酸中毒的改善可减少肾内皮素的生成和肾损伤并且可更好地维持GFR
Amelioration of metabolic acidosis in patients with low GFR reduced kidney endothelin production and kidney injury, and better preserved GFR
Phisitkul, S, Khanna, A, Simoni, J   2010/10/22 15:16:39 
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Kidney Int , 2010,
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Metabolic acidosis often accompanies low glomerular filtration rate and induces secretion of endothelin, which in turn might mediate kidney injury. Here we tested whether treatment of metabolic acidosis in patients with low glomerular filtration rate reduced the progression of kidney disease. Fifty-nine patients with hypertensive nephropathy and metabolic acidosis had their blood pressure reduced with regimens that included angiotensin-converting enzyme inhibition. Thirty patients were then prescribed sodium citrate, and the remaining 29, unable or unwilling to take sodium citrate, served as controls. All were followed for 24months with maintenance of their blood pressure reduction. Urine endothelin-1 excretion, a surrogate of kidney endothelin production, and N-acetyl-β-d-glucosaminidase, a marker of kidney tubulointerstitial injury, were each significantly lower, while the rate of estimated glomerular filtration rate decline was significantly slower. The estimated glomerular filtration rate was statistically higher after 24months of sodium citrate treatment compared to the control group. Hence it appears that sodium citrate is an effective kidney-protective adjunct to blood pressure reduction and angiotensin-converting enzyme inhibition.
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病例分析 <span class="ModTitle_Intro_Right" id="EPMI_Home_MedicalCases_Intro_div" onclick="javascript:window.location='http://www.elseviermed.cn/tabid/127/Default.aspx'" onmouseover="javascript:document.getElementById('EPMI_Home_MedicalCases_Intro_div').style.cursor='pointer';document.getElementById('EPMI_Home_MedicalCases_Intro_div').style.textDecoration='underline';" onmouseout="javascript:document.getElementById('EPMI_Home_MedicalCases_Intro_div').style.textDecoration='none';">[栏目介绍]</span>  病例分析 [栏目介绍]

 王燕燕 王曙

上海交通大学附属瑞金医院内分泌科

患者,女,69岁。2009年1月无明显诱因下出现乏力,当时程度较轻,未予以重视。2009年3月患者乏力症状加重,尿色逐渐加深,大便习惯改变,颜色变淡。4月18日入我院感染科治疗,诉轻度头晕、心慌,体重减轻10kg。无肝区疼痛,无发热,无腹痛、腹泻、腹胀、里急后重,无恶性、呕吐等。入院半月前于外院就诊,查肝功能:ALT 601IU/L,AST 785IU/L,TBIL 97.7umol/L,白蛋白 41g/L,甲状腺功能:游离T3 30.6pmol/L,游离T4 51.9pmol/L,心电图示快速房颤。
 

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