Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Structural distortion of glomerular capillaries in chronic rat Masugi nephritis was studied by light, transmission electron, and scanning electron microscopy. A few months after rats were given injections of heterologous nephrotoxic antibodies, focal and local mesangial as well as basement membrane thickenings were observed. Using scanning electron microscopy, glomerular corrosion castings disclosed that definite loop constriction with occasional gaps occurred in such local foci. The local changes were gradually extended to adjacent areas in rats with severe proteinuria, later resulting in a broad disappearance of the loops. Also observed were glomeruli undergoing a collapse with structural simplification resulting from multiple loss of communicating branches. At the terminal stage, almost all glomeruli were involved in varying degrees in either of these changes. In contrast, no progression of the disease process was observed in rats with minimal proteinuria. By scanning electron microscopy, a large number of castings from various angles revealed that morphologically normal glomeruli were involved in local and ultimately global obsolescence under the condition of persistent proteinuria.
 ...
PMID:Structural distortion of glomerular capillary loops in the chronic phase of rat Masugi nephritis. 43 55

We analysed the sequence of structural changes leading to focal segmental glomerulosclerosis (FSGS) in chronic Masugi nephritis. The protocol resulted in an immediate onset of the disease and the development of segmental sclerosis in a considerable proportion of glomeruli within 28 days of serum injection. Throughout the study, the degree of structural damage was significantly correlated with protein excretion. Even 1 day after injection of the serum, the whole spectrum of early lesions was encountered involving all three cell types. Endothelial detachments, mesangiolysis and podocyte foot process effacement were most prominent. There was focal persistence of capillary microthrombosis but, generally, mesangial and endothelial injuries recovered. The development of podocyte lesions was different: on one hand recovery was seen leading to the re-establishment of an interdigitating foot process pattern, and on the other persistent podocyte detachments from peripheral capillaries allowed the attachment of parietal epithelial cells to "naked" portions of the glomerular basement membrane (GBM), and thus to the formation of a tuft adhesion to Bowman's capsule. Progressive podocyte degeneration at the flanks of an adhesion permitted expansion of the adhesion by encroachment of parietal cells onto the tuft along the denuded GBM. Inside an adhesion, capillaries and mesangial areas either collapse or become obstructed by hyalinosis or thrombosis. Resident cells disappear progressively from inside an adhesion; macrophages may invade. Segmental sclerosis in this model consists of collapsed tuft structures adhering broadly to the cortical interstitium. Proliferation of mesangial cells did not contribute to this development. Recovery of endothelial and mesangial lesions was associated with cell proliferation in early stages of the disease; podocyte proliferation was not encountered at any stage. We conclude that the inability to replace an outmatched podocyte crucially underlies the development of sclerosis. Severe podocyte damage cannot be repaired but leads to tuft adhesions to Bowman's capsule followed by progressive collapse of tuft structures inside an adhesion, resulting in segmental glomerulosclerosis.
 ...
PMID:The development of focal segmental glomerulosclerosis in masugi nephritis is based on progressive podocyte damage. 897 62