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The opisthonephric kidney of larval anadromous sea lamprey, Petromyzon marinus L., undergoes a programmed regression during metamorphosis. Degeneration is initiated in the anterior end of each kidney and progresses posteriorly until the kidneys are reduced to short, pigmented strands by the end of metamorphosis. The first sign of degeneration in both the epithelium of the renal corpuscles and the tubules is a folding of the basal lamina. Autolysis then occurs throughout the entire epithelium of the nephron with the gradual accumulation of larger and greater numbers of acid phosphatase-containing autophagic vacuoles, cytosomes, and myelin figures. Cytoplasmic debris and electron-dense material accumulates in the tubular lumina and in the urinary space. Although no definitive evidence is provided for the method of removal of the tubular epithelium, macrophages play a large part in the phagocytosis of the components of the renal corpuscle. Mesangial cells appear to engulf debris from the capillaries while a second type of macrophage is involved in the destruction of podocytes and parietal epithelial cells. The method of programmed degeneration of the renal corpuscle closely resembles descriptions of the mammalian renal corpuscle in diseased conditions. The sole surviving element of the degeneration of the entire nephron epithelium is a pleated basal lamina. The regressing larval opisthonephros has potential as an alternative system for studying a normal developmental pattern such as tissue regression.
The opisthonephric kidney of larval anadromous sea lamprey, Petromyzon marinus L., undergoes a programmed regression during metamorphosis. Degeneration is initiated in the anterior end of each kidney and progresses posteriorly until the kidneys are reduced to short, pigmented strands by the end of metamorphosis. The first sign of degeneration in both the epithelium of the renal corpuscles and the tubules is a folding of the basal lamina. Autolysis then occurs throughout the entire epithelium of the nephron with the gradual accumulation of larger and greater numbers of acid phosphatase-containing autophagic vacuoles, cytosomes, and myelin figures. Cytoplasmic debris and electron-dense material accumulates in the tubular lumina and in the urinary space. Although no definitive evidence is provided for the method of removal of the tubular epithelium, macrophages play a large part in the phagocytosis of the components of the renal corpuscle. Mesangial cells appear to engulf debris from the capillaries while a second type of macrophage is involved in the destruction of podocytes and parietal epithelial cells. The method of programmed degeneration of the renal corpuscle closely resembles descriptions of the mammalian renal corpuscle in diseased conditions. The sole surviving element of the degeneration of the entire nephron epithelium is a pleated basal lamina. The regressing larval opisthonephros has potential as an alternative system for studying a normal developmental pattern such as tissue regression.
A systematic ultrastructural analysis of proximal tubule atrophy and cortical interstitial changes was carried out in human chronic nephropathy. The investigation was based on human hydronephrotic kidneys, which had been surgically removed and subsequently perfusion-fixed for light and electron microscopy. Normal kidney tissue, which was derived from nephrectomy specimens with pathological changes confined to part of the kidney or to the renal pelvis, was used for control material. A slight degree of proximal tubule atrophy was characterized by reduction of mitochondria and basolateral membranes, enlargement of large endocytic vacuoles and increased numbers of lysosomes containing lamellar material. In moderate atrophy these changes were further accentuated, and in addition there was an increasing loss of microvilli and a reduction of endocytic invaginations and small endocytic vacuoles. In severe atrophy all types of organelles were sparse and the architecture of the tubule cells greatly simplified. A distinctive feature of atrophic tubules was the presence in the tubule cells of large bundles of actin-like filaments, which were often associated with outpouchings of basal cell parts and basement membrane. The reduction of mitochondria and basolateral cell membranes and the changes of endocytic vacuoles and lysosomes indicate that proximal tubule atrophy also in early stages may be associated with impairment of tubular transport processes. Comparisons with previous observations in various types of experimentally induced tubule cell degeneration and with the ultrastructure of regenerating proximal tubule cells provide some evidence that degenerative changes as well as imperfect regeneration of tubule cells may contribute to the alterations of ultrastructure in tubular atrophy. It is suggested that changes of the cortical interstitium may be of pathogenic importance for the progression of tubular atrophy by altering the spatial relationships between tubules and capillaries.
It is not clear whether tubular cell necrosis is present or not in acute renal failure (ARF) of ischaemic type ("acute tubular necrosis"). In order to get quantitative data, using precisely defined criteria for tubular cell necrosis, 25 renal biopsies from 24 patients with ARF (11 obtained in the active phase, 14 in the early recovery period) were compared with 12 control biopsies. In all 1959 proximal cells and 1603 distal cells were analysed by electron microscopy. Cellular disintegration was very rare in all groups. Shrinkage necrosis (apoptosis) was not present in the proximal tubules of the controls and was rare in ARF (1.6-2.1%). In the distal tubules of controls 2.7% of all cells showed shrinkage necrosis. The incidence in ARF was not significantly increased. "Non-replacement sites" in distal tubules (probably loci where cells have recently been desquamated) were significantly increased in number (5.2%) in the active phase in ARF compared to controls and recovery. The relative number of regenerating cells was not increased. These data show that there is no widespread necrosis of tubular cells in ARF. The increased incidence in distal tubules of focal, denuded areas of the basement membrane in the active phase of ARF indicates a slightly increased desquamation of cells and/or a failure to cover such sites by adjacent cells. This process is not restricted to the brief induction phase of ARF but continues during the whole active phase.
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