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Titolo:
Enhanced interstitial expression of caldesmon in IgA nephropathy and its suppression by glucocorticoid-heparin therapy
Autore:
Ando, Y; Moriyama, T; Oka, K; Takatsuji, K; Miyazaki, M; Akagi, Y; Kawada, N; Isaka, Y; Izumi, M; Yokoyama, K; Yamauchi, A; Horio, M; Ando, A; Ueda, N; Sobue, K; Imai, E; Hori, M;
Indirizzi:
Osaka Prefectural Coll Nursing, Osaka, Japan Osaka Prefectural Coll Nursing Osaka Japan l Coll Nursing, Osaka, Japan Nara Inst Sci & Technol, Nara, Japan Nara Inst Sci & Technol Nara JapanNara Inst Sci & Technol, Nara, Japan
Titolo Testata:
NEPHROLOGY DIALYSIS TRANSPLANTATION
fascicolo: 6, volume: 14, anno: 1999,
pagine: 1408 - 1417
SICI:
0931-0509(199906)14:6<1408:EIEOCI>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN RENAL FIBROBLASTS; SMOOTH MUSCLE ACTIN; MYOFIBROBLASTS; FIBROSIS; GLOMERULONEPHRITIS; PROGRESSION; DISEASE; DIFFERENTIATION; ACTIVATION; MODULATION;
Keywords:
caldesmon; glucocorticoid heparin therapy; IgA nephropathy; interstitial cell; myofibroblast; phenotypic change;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Imai, E Osaka&Univ,65,h Med A8,Biomed Res Ctr,Dept Clin Lab Sci, Dept Internal Med Osaka Univ 2-2 Yamadaoka Suita Osaka Japan 565 , Dept Internal Med
Citazione:
Y. Ando et al., "Enhanced interstitial expression of caldesmon in IgA nephropathy and its suppression by glucocorticoid-heparin therapy", NEPH DIAL T, 14(6), 1999, pp. 1408-1417

Abstract

Background. With progressive renal disease, structural derangement increasingly encompasses the tubulointerstitial compartment. Tubulointerstitial injury is a critical determinant of renal functional reserve and prognosis inrenal disease. Interstitial cells acquiring characteristic of myofibroblasts are an important contributor to interstitial fibrosis. Caldesmon, a calmodulin or actin binding protein, is a molecular marker of differentiation in smooth muscle cells and has recently been shown by us to be a good markerof mesangial cell activation in IEA nephropathy patients. Methods. We studied whether the expression of caldesmon in interstitium ofthe kidney was enhanced in the process of glomerular disease and whether it would be a marker of interstitial activation in specific disease states. We performed immunohistochemical staining with anti-caldesmon antibodies in38 biopsy specimens from IEA nephropathy patients and analysed them quantitatively with a computer-aided manipulator. Interstitial caldesmon expression were compared with histological changes and clinical parameters. Results. Caldesmon expression was enhanced where interstitial cell infiltration and fibrosis were found. Immunoelectron microscopy revealed that caldesmon staining in the renal interstitium was cytoplasmic, and in the processes of myofibroblast-like cells. Caldesmon expression was more prominent inthe intense CD68 infiltrated group than in the low positive cells infiltrated group. Patients showing high intensity of interstitial caldesmon expression had significantly higher urinary protein excretion than those showing low intensity of caldesmon expression. Next, 15 patients were treated with glucocorticoid and heparin for 4-8 weeks and re-biopsies were performed. Caldesmon expression was reduced in concomitant with decreased interstitial cell infiltration. Follow-up of these patients (average 24 months) revealed a significant suppression of urinary protein excretion and significant improvement of creatinine clearance. Conclusion. These results suggest that the interstitial caldesmon expression is associated with the progression of IgA nephropathy, and glucocorticoid heparin therapy may reverse the phenotypic change of interstitial cells during the disease process of glomerulonephritis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 13:59:25