Rasch Ruth, Nyengaard Jens R, Marcussen Niels, Meyer Timothy W
Department of Cell Biology, Stereological Research and Electron Microscopy Laboratory, University of Aarhus, Aarhus, Denmark.
Kidney Int. 2002 Aug;62(2):496-506. doi: 10.1046/j.1523-1755.2002.00481.x.
Rats 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.
Stereologic studies were performed 10 weeks after administration of puromycin (PAN) or saline (Cont). Serial sections were examined to assess glomerular structure.
Rats 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 x 10(6) microm3; Cont, 2.07 +/- 0.47 x 10(6) microm3), 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.
Acute 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.
从急性嘌呤霉素肾病中恢复的大鼠随后会出现广泛的肾小球和肾小管间质损伤。本研究旨在确定恢复期出现的可能引发进行性肾脏疾病的结构变化。
在给予嘌呤霉素（PAN）或生理盐水（对照）10周后进行体视学研究。检查连续切片以评估肾小球结构。
接受嘌呤霉素的大鼠出现大量蛋白尿，在10周时几乎恢复到对照水平。这些动物的肾脏中度肿大，间质扩张（PAN组，254±47mm³；对照组，152±23mm³；P<0.05）。平均肾小球体积与对照组无差异（PAN组，1.90±0.38×10⁶μm³；对照组，2.07±0.47×10⁶μm³），但在PAN大鼠中发现了约一半正常大小的肾小球亚群。连续切片显示，这些肾小球中的大多数与正常肾小管节段不相连。连续切片还显示，从肾病中恢复的大鼠中，超过90%的肾小球有粘连将肾小球毛细血管丛与鲍曼囊相连。在PAN动物中，粘连平均占鲍曼囊表面的8±11%，而在对照组中占表面的不到1%。粘连的出现与每个肾小球中脏层或壁层上皮细胞的平均数量减少无关。
急性嘌呤霉素肾病不会导致脏层上皮细胞数量显著减少。然而，蛋白尿缓解后，存在以肾小球毛细血管丛与鲍曼囊之间粘连为特征的广泛肾小球损伤。这种残留肾小球损伤的进展可能导致急性肾病恢复后肾小球节段性硬化的后期发展。
