A distinctive segmental glomerular abnormality is confined to the region of the tubular opening. The hypothesis was that this followed
prolapse of the tuft into the tubule. Analysis was made of 39 renal biopsy specimens with acute postinfective
glomerulonephritis, later material from ten cases, four specimens from three women with
pre-eclampsia, and 21 control specimens, with morphometry of glomeruli and immunohistological examination for
immunoproteins and monocytes/macrophages.
Prolapse was found in 14 specimens with acute postinfective
glomerulonephritis, associated in eight with adhesion to Bowman's capsule and local alterations in the tuft, which together constitute early tip changes. Another three had early tip changes only and eight others had thin adhesions between the tuft and
capsule next to the tubular opening. Later material confirmed this order of development and showed another late change, with sclerosed and hyaline material in the tuft and adhesion at the tubular origin. Findings in
pre-eclampsia were comparable. Glomeruli were significantly larger in acute postinfective
glomerulonephritis than in controls and were shown by others to be larger in
pre-eclampsia than in normal pregnancy. Immunohistology showed
IgM and a few foamy monocytes/macrophages in early tip changes but not in prolapsed loops. Glomerular
prolapse appears to be a temporary consequence of acute enlargement of the tuft, probably causes mechanical damage to epithelial cells, and is a precursor of permanent structural changes near the tubular origin. This gives a unifying hypothesis to explain how these changes can be seen in acute postinfective
glomerulonephritis,
pre-eclampsia, and many other human and experimental renal disorders.