SCANNING AND TRANSMISSION ELECTRON-MICROSCOPIC COMPARISON OF PUROMYCIN AMINONUCLEOSIDE-INDUCED NEPHROSIS TO HYPERALBUMINEMIA-INDUCED PROTEINURIA WITH EMPHASIS ON KIDNEY PODOCYTE PEDICEL LOSS

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  • 1 January 1977
    • journal article
    • research article
    • Vol. 36  (2) , 183-197
Abstract
Ultrastructural changes in the visceral epithelium and proximal tubules of rats were studied by scanning and transmission electron microscopy during the onset and progression of puromycin aminonucleoside nephrosis (PAN)-induced proteinuria. These changes were compared with those that occur during a similar degree of proteinuria induced by i.p. injections of albumin. With the onset of proteinuria and oliguria, PAN rats exhibited loss of podocyte pedicels and podocyte major processes, an increase in pinocytotic activity and an accumulation of cytoplasmic vacuoles and granules of variable size, shape and electron density. Loss of podocyte pedicels involved a gradual decrease in pedicel height beginning at the pedicel tip and progressing down the pedicel arm, formation of nublike protrusions and interpedicel microbridges (35-45 nm in width and 40-60 nm in length) along the pedicel''s base, the merging of microbridges to form more extensive regions of interpedicel contact and a gradual broadening and retraction of pedicels. In response to hyperalbuminemia-induced proteinuria, kidney podocytes exhibited an increase in pinocytotic activity and an accumulation of protein absorption droplets. Unlike the reactions during PAN, however, the podocyte pedicels, slit pores and major processes of rats with hyperalbuminemia-induced proteinuria remained discrete. The loss of pedicels and major processes during PAN apparently resulted from the effects of puromycin aminonucleoside per se rather than from the proteinuria associated with this disease. The proximal tubules of rats with hyperalbuminemia-induced proteinurea exhibit the same characteristic changes as PAN rat proximal tubules (i.e., loss of brush border, dilated lumina, abnormally thin walls and accumulation of periodic acid-Schiff positive electron-dense luminal casts and cytoplasmic protein absorption droplets). The significance of these ultrastructural findings during PAN and hyperalbuminemia-induced proteinuria were discussed in terms of the etiology of PAN.