Harvey J M, Howie A J, Lee S J, Newbold K M, Adu D, Michael J, Beevers D G
Department of Medicine, Dudley Road Hospital, Birmingham.
Lancet. 1992 Dec 12;340(8833):1435-6. doi: 10.1016/0140-6736(92)92624-o.
27 patients with hypertension and persistent proteinuria were investigated by renal biopsy. The 13 patients without structural glomerular abnormalities were younger and had less proteinuria than the other 14, but otherwise the two groups had similar clinical features. 6 of the 14 had diffuse glomerular abnormalities; the other 8 had segmental sclerosing lesions, which were mainly in the hilum of the glomeruli, as seen in states of glomerular overload. Glomeruli in all groups were larger than those in normotensive people. It is possible that hypertension causes glomerular enlargement, proteinuria, and segmental glomerular lesions because of loss of functioning glomeruli due to ischaemia.
对27例高血压伴持续性蛋白尿患者进行了肾活检。13例无肾小球结构异常的患者比另外14例患者更年轻,蛋白尿也更少,但两组在其他方面具有相似的临床特征。14例患者中有6例存在弥漫性肾小球异常;另外8例有节段性硬化性病变,主要位于肾小球肾门处,如在肾小球超负荷状态下所见。所有组的肾小球均比血压正常者的肾小球大。高血压可能由于缺血导致功能性肾小球丧失,从而引起肾小球增大、蛋白尿和节段性肾小球病变。