Glomerular alterations in an ischemic model of acute renal failure

J. L. Barnes, R. W. Osgood, H. J. Reineck, J. H. Stein

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

One hour of total renal ischemia in the rat is associated with diminished glomerular filtration rate, a reduction in renal flow, and oliguira. A number of mechanisms including back-leakage of tubular filtrate, obstruction, and hemodynamic alterations have been postulated to be responsible for the reduced glomerular filtration rate in acute renal failure. Most emphasis has been placed on tubular changes following renal ischemia, and little attention has been focused on glomerular changes during early reflow. Since glomerular damage may account for a portion of function impairment during reflow, studies were performed to examine glomerular morphology in this model of acute renal failure. Glomerular alterations, as noted by scanning and transmission electron microscopy, were progressive spring reflow. At 30 minutes following 1 hour of renal ischemia, scanning electron microscopy revealed focal spreading of podocyte cell bodies associated with loss of foot processes and increased numbers of microvillous projections. Also, numerous cytoplasmic protuberances were observed on the epithelial cell surface. Transmission electron microscopy confirmed these changes and revealed displacement and duplication of slit diaphragms. In addition, endothelial fenestrae were reduced in number and appeared unduly wide. At 30 minutes, glomerular polyanion, determined by colloidal iron staining, was unchanged in ischemic kidneys when compared with the untouched contralateral control. At 1 hour of reflow, the above described glomerular morphologic changes were diffuse and global in distribution. However, cytoplasmic protuberances were uncommon. Changes in the glomerular epithelial slit pore complex at this time included loss of slit diaphragms and abnormal widening of slit pores. Also, glomerular polyanion was markedly diminished when compared with controls. These glomerular changes have not been previously described during early reflow in the ischemic model of acute renal failure. The role these alterations have in loss of renal function is not known; however, a loss of surface area available for ultrafiltration is suggested. In addition, loss of the glomerular polyanion suggests an increased permeability to macromolecules.

Original languageEnglish (US)
Pages (from-to)378-386
Number of pages9
JournalLaboratory Investigation
Volume45
Issue number4
StatePublished - Dec 1 1981

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology

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