Renal structural abnormalities following recovery from acute puromycin nephrosis.
Renal structural abnormalities following recovery from acute puromycin nephrosis.
复制标题
急性嘌呤霉素肾病恢复后的肾脏结构异常。
DOI：
10.1046/j.1523-1755.2002.00481.x
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Meyer,TimothyW
中科院分区：
文献类型：
--
作者：
Rasch,Ruth;Nyengaard,JensR;Marcussen,Niels;Meyer,TimothyW
Renal structural abnormalities following recovery from acute puromycin nephrosis.BackgroundRats that recover from acute puromycin nephrosis later develop widespread glomerular and tubulointerstitial injury. The current study sought to identify structural changes present in the recovery phase that could precipitate progressive renal disease.MethodsStereologic studies were performed 10 weeks after administration of puromycin (PAN) or saline (Cont). Serial sections were examined to assess glomerular structure.ResultsRats receiving puromycin developed heavy proteinuria that returned nearly to control levels at 10 weeks. Kidneys in these animals were moderately enlarged and exhibited expansion of the interstitium (PAN, 254 ± 47 mm3; Cont, 152 ± 23 mm3;P< 0.05). The average glomerular volume was not different from control (PAN, 1.90 ± 0.38 × 106μm3; Cont, 2.07 ± 0.47 × 106μm3), but a subpopulation of glomeruli of about half normal size was found in PAN rats. Serial sections revealed that most of these glomeruli were not connected to normal tubule segments. Serial sections also revealed that more than 90% of glomeruli in rats recovering from nephrosis had synechias joining the tuft to Bowman's capsule. Synechias occupied an average of 8 ± 11% of the Bowman's capsule surface in PAN animals versus less than 1% of the surface in controls. The appearance of synechias was not associated with a reduction in the mean number of visceral or parietal epithelial cells per glomerulus.ConclusionsAcute puromycin nephrosis does not cause a notable reduction in visceral epithelial cell number. However, widespread glomerular injury characterized by synechia between the tuft and Bowman's capsule is present following remission of proteinuria. Progression of this residual glomerular injury could contribute to the late development of glomerular segmental sclerosis following recovery from acute nephrosis.
