Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

8 cases of membranous glomerulonephritis (MG) after renal transplants (RT) are presented; one being a recurrence of the original disease and the other 7 due to a different cause of renal insufficiency. The total incidence of MG after transplantation was 1.63%; 1.39% being the incidence of MG of new cases. Only 1 patient showed decrease of renal function and in this case the MG was accompanied by chronic rejection lesions. There was no sign of neoplasias nor drugs producing MG. As far as chronic infections are concerned, only one patient showed B antigen and it was not observed during the immunofluorescent test in the biopsy. 6 patients had urological complications after the renal transplant (3 cases of urinary fistula; 2 cases of obstructive uropathy; 1 case of short ureter). 2 patients experienced the start of hemodialysis due to focal and segmentary glomerulosclerosis. The beginning of proteinuria commences between 2 and 23 months after the RT (median 13,0 +/- 7,5 moths); with a range of between 2.0 and 12.0 gr/day (median: 6.8 +/- 3,2 Z gr/day), this being nephrotic in 4 cases. Proteinuria improved 1 case, and persisted in the other patients at the same level registered previous to the diagnosis. MG is a non-frequent complication or RT and is usually benign. Patients with post-transplant urologic complications could be considered to have a higher risk of developing a MG "de novo".
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PMID:[Membranous nephritis after renal transplantation]. 189 4

Tubular cell damage is an important mediator of interstitial fibrosis in chronic renal diseases. Glomerular and tubular damage in genetic hypertension was therefore studied. Tubular and glomerular damage was investigated in 10-, 40-, and 70-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) and compared with glomerular capillary pressure (P(GC)) and glomerulosclerosis in superficial (OC) and juxtamedullary (JMC). Tubular vimentin was used as criterion of tubular damage. Variation in tubular diameter was measured during change in perfusion pressure, and ureter ligation was used to demonstrate the relationship between tubular pressure and appearance of vimentin-positive cells. Tubular and glomerular damage was most pronounced in JMC and greater in SHR than in WKY. It was absent in 10-wk-old WKY and significantly higher in JMC of SHR compared with WKY at 70 wk of age. Numbers of vimentin-positive segments were 18 +/- 9 vs. 38 +/- 7% in JMC of 70-wk-old WKY and SHR (P < 0.02), and glomerulosclerosis was seen in 8 +/- 3 vs. 19 +/- 5% of glomeruli in JMC of 70-wk-old WKY and SHR, respectively (P < 0.01). P(GC) was 45 +/- 3 mmHg in JMC of WKY and 57 +/- 3 mmHg in JMC of 70-wk-old SHR (P < 0.001). Tubular diameter variation was greatest in SHR (P < 0.05) during pressure variation. Proteinuria was present only in 40- and 70-wk-old SHR and did not correlate with tissue damage. Tubular and glomerular damage in both strains develops in parallel and may be caused by a common mechanism, which may be glomerular capillary and tubular wall stretch during acute blood pressure variation which is greatest in JMC in SHR.
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PMID:Glomerular and tubular damage in normotensive and hypertensive rats. 1553 68