Wagner P K, Pippig L, Thoenes W
Klin Wochenschr. 1979 Feb 1;57(3):135-42. doi: 10.1007/BF01476054.
A 38-year-old female patient developed a Pseudo-Bartter's-Syndrome with hypokalemic alkalosis, hyponatremia and hyperrenism as the result of the abuse of diuretics (furosemide, spironolactone, thiabutacide) for a period of more than 10 years. The needle biopsy specimen from the kidney showed a hyperplasia of the juxtaglomerular apparatus and of the mesangium cells as the morphologic basis of hyperrenism, a focal vacuolisation of the proximal tubular epithelium and a focal atrophy of the distal tubules. The pathogenesis of the tubular alterations and their possible relation to hypokalemia, hypoxemia or drug-toxicity is discussed, a satisfactory interpretation, however, cannot be given. The encroachment of proximal tubular epithelium on the parietal layer of Bowman's capsule is another striking pathoanatomical finding, and considered a compensatory mechanism under the continuous loss of water.
一名38岁女性患者因滥用利尿剂（速尿、螺内酯、丁苯氧酸）超过10年，出现了伴有低钾性碱中毒、低钠血症和高肾素血症的假性巴特综合征。肾脏穿刺活检标本显示肾小球旁器和系膜细胞增生，这是高肾素血症的形态学基础，近端肾小管上皮细胞局灶性空泡化以及远端肾小管局灶性萎缩。文中讨论了肾小管改变的发病机制及其与低钾血症、低氧血症或药物毒性的可能关系，但无法给出令人满意的解释。近端肾小管上皮细胞向鲍曼囊壁层的侵入是另一个显著的病理解剖学发现，被认为是在持续失水情况下的一种代偿机制。
