Abstract

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.

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