Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tubulointerstitial nephritis and glomerulonephritis were produced in Brown-Norway rats (BN) by a single immunization with 2 mg of lyophilized bovine glomerular basement membrane. Tubulointerstitial nephritis was evident before glomerulonephritis. Antibody first bound to tubular basement membranes (TBM), and then the renal cortex was infiltrated with inflammatory cells. The TBM was split, and many renal tubules, especially proximal tubules, were destroyed. Approximately 14 days after the beginning of the tubular phase, antibody was observed to be bound to glomerular basement membranes (GBM) in linear fashion. There was epithelial and mesangial cell proliferation, splitting and reduplication of GBM, crescent formation, and glomerular scarring and atrophy.
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PMID:Tubulointerstitial nephritis and glomerulonephritis in Brown-Norway rats immunized with heterologous glomerular basement membrane. 87 71

Tubulointerstitial nephritis, regularly induced in Brown Norway rats by autosensitization with tubular basement membranes, appeared acutely at about 10 days and was completely inhibited by Cyclosporin A (CyA) when this was given before and at the time of onset of the disease. It did not recur after the end of therapy. In spite of this disease inhibition, autoantibodies against tubular basement membranes persisted in the circulation and in the kidney. It is therefore suggested that it is not so much the antibodies that are the decisive factors in the pathogenesis of this and other autoimmune diseases but, rather cellular factors that are directly influenced by CyA. Although in this model CyA application was a preventive measure, the experiments provide a cogent reason for the application of CyA as early as possible in acute and seriously damaging diseases.
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PMID:Cyclosporin A inhibits autoimmune experimental tubulointerstitial nephritis. 369 36