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Titolo:
Renovascular hypertension does not influence repair of glomerular lesions induced by anti-thymocyte glomerulonephritis
Autore:
Wenzel, UO; Wolf, G; Thaiss, F; Helmchen, U; Stahl, RAK;
Indirizzi:
Univ Hamburg Hosp, Dept Med, Div Nephrol, Hamburg, Germany Univ Hamburg Hosp Hamburg Germany pt Med, Div Nephrol, Hamburg, Germany Univ Hamburg Hosp, Dept Pathol, Hamburg, Germany Univ Hamburg Hosp Hamburg Germany g Hosp, Dept Pathol, Hamburg, Germany
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 3, volume: 58, anno: 2000,
pagine: 1135 - 1147
SICI:
0085-2538(200009)58:3<1135:RHDNIR>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; MESANGIAL PROLIFERATIVE GLOMERULONEPHRITIS; IMMUNE-COMPLEX NEPHRITIS; CELL-PROLIFERATION; RENAL INJURY; RATS; EXPRESSION; MACROPHAGES; HYPERTROPHY; PROGRESSION;
Keywords:
glomerulosclerosis; cell proliferation; monocytes; tubulointerstitial damage; proteinuria; blood pressure;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Wenzel, UO Univ Hamburg, Dept Med, Div Nephrol, Pav 61,Martinistr 52, D-20246 Hamburg, Germany Univ Hamburg Pav 61,Martinistr 52 Hamburg Germany D-20246 many
Citazione:
U.O. Wenzel et al., "Renovascular hypertension does not influence repair of glomerular lesions induced by anti-thymocyte glomerulonephritis", KIDNEY INT, 58(3), 2000, pp. 1135-1147

Abstract

Background. Systemic hypertension is a risk factor for progression of renal disease. However, it is not clear whether hypertension has an effect on healing or regression of immune-mediated glomerular damage. To evaluate thiseffect, we applied a model of glomerulonephritis in rats with two-kidney, one-clip hypertension and studied the effect of hypertension on the healingprocess of this nephritis. Methods. The anti-thymocyte serum (ATS) glomerulonephritis was induced in rats six weeks after initiation of two-kidney, one-clip hypertension, when blood pressure was already increased. Renal structure and unction were examined six weeks later. Glomerular expression of or smooth muscle actin, the cell cycle inhibitor p27(Kip1), and transforming growth factor-p (TGF-beta)was evaluated by Western blotting. Glomerular proliferation, monocyte infiltration, and fibronectin were examined by immunohistochemistry. Results. Decreased survival, an increase of proteinuria, as well as increased glomerular and tubulointerstitial damage, were found in hypertensive rats compared with normotensive rats. Expression of fibronectin, or-smooth muscle actin, TGF-beta, and p27(Kip1) was increased in the nonclipped kidney. Complete healing of the glomerular changes associated with the nephritis occurred in normotensive nephritic rats. Surprisingly, complete healing of the nephritis was also found in the clipped as well as nonclipped kidneys ofrenovascular hypertensive rats. No significant differences could be found for survival, proteinuria, glomerular size, proliferation, monocyte/macrophage infiltration, sclerosis, tubulointerstitial damage, as well as expression of or-smooth muscle actin, TGF-beta, fibronectin, and p27(Kip1) between hypertensive rats with and without nephritis. Conclusion. These data demonstrate that renovascular hypertension does notinfluence healing of the glomerular lesions in the anti-thymocyte serum nephritis. This is a rather surprising observation and leaves the question open of which role, in acute glomerulonephritis, or whether its role depends on the type of glomerulonephritis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 20:46:22