Murray S M
J Pathol. 1979 Aug;128(4):203-11. doi: 10.1002/path.1711280406.
The progress of serotonin-induced renal lesions was studied over a period of 6 mth following a single intraperioneal injection of 40 mg/kg serotonin. The predominant lesion was ischaemic necrosis of tubules of patchy distribution. Parahilar areas were usually spared and a narrow subcapsular strip was less severely affected than deeper parts. The early tubular lesions appeared to be an accelerated form of the lesion of complete renal ischaemia. The necrotic tubules were soon relined by epithelium from surviving segments and became dilated. This phase of dilatation corresponded approximatly with the period of diuresis following serotonin injection and was followed by collapse and atrophy of tubules. Possible mechanisms concerned in the sequential appearance of tubular dilatation and collapse were discussed. Many collapsed tubules eventually atrophied and were associated with basement membrane thickening and round cell infiltration. Reflux of necrotic proximal tubule cytoplasm into glomerular capsular spaces occurred in the early stages of the lesion. This lesion is not specific for serotonin nephropathy and can be produced by allowing normal rat kidney to autolyse.
在单次腹腔注射40mg/kg血清素后的6个月期间,对血清素诱导的肾损伤进展进行了研究。主要病变是散在分布的肾小管缺血性坏死。肾门周围区域通常未受影响,肾包膜下的狭窄条带比深部区域受影响较轻。早期肾小管病变似乎是完全性肾缺血病变的一种加速形式。坏死的肾小管很快被存活节段的上皮重新覆盖并扩张。这种扩张阶段大致与血清素注射后的利尿期相对应,随后是肾小管的塌陷和萎缩。讨论了肾小管扩张和塌陷相继出现的可能机制。许多塌陷的肾小管最终萎缩,并伴有基底膜增厚和圆形细胞浸润。在病变早期,坏死近端肾小管的细胞质反流到肾小球囊腔。这种病变并非血清素肾病所特有,正常大鼠肾脏自溶也可产生。