HOLLIDAY M A, BRIGHT N H, SCHULZ D, OLIVER J
J Exp Med. 1961 Jun 1;113(6):971-80. doi: 10.1084/jem.113.6.971.
Acute chloride depletion in rats is associated with the occurrence of an extensive cell damage in the mid-portion of the proximal convolutions which is followed by an excessive hyperplastic reaction of the renal epithelium; no other significant lesions were found by microdissection in either the tubules of the nephrons or the collecting system. Potassium deficiency is not essential to the development of this lesion but does increase the severity of the reaction. As in the case of potassium deficiency, chloride depletion predisposes to or exaggerates the structural alterations that accompany excess phosphate intake. The relations of the different structural changes in renal architecture that occur in various states of electrolyte imbalance are discussed as well as the relation of the lesions seen experimentally in the rat and monkey and clinically in man.
大鼠急性氯化物缺乏与近端曲部中段广泛的细胞损伤有关,随后是肾上皮的过度增生反应;通过显微解剖在肾单位的肾小管或集合系统中均未发现其他明显病变。钾缺乏对该病变的发展并非必不可少,但会增加反应的严重程度。与钾缺乏的情况一样,氯化物缺乏易引发或加剧伴随过量磷酸盐摄入的结构改变。文中讨论了在各种电解质失衡状态下肾结构中不同结构变化之间的关系,以及在大鼠和猴子身上实验观察到的病变与人类临床病变之间的关系。