Glomerulonephritis

被引:163
作者
Chadban, SJ
Atkins, RC
机构
[1] Royal Prince Alfred Hosp, Camperdown, NSW 2050, Australia
[2] Monash Med Ctr, Dept Nephrol, Clayton, Vic 3168, Australia
[3] Univ Sydney, Camperdown, NSW, Australia
关键词
D O I
10.1016/S0140-6736(05)66583-X
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The term glomerulonephritis encompasses a range of immune-mediated disorders that cause inflammation within the glomerulus and other compartments of the kidney. Studies with animal models have shown the crucial interaction between bone-marrow-derived inflammatory cells and cells intrinsic to the kidney that is both fundamental and unique to the pathogenesis of glomerulonephritis. The mechanisms of interaction between these cells and the mediators of their coordinated response to inflammation are being elucidated. Despite these pathophysiological advances, treatments for glomerulonephritis remain non-specific, hazardous, and only partly successful. Glomerulonephritis therefore remains a common cause of end-stage kidney failure worldwide. Molecule-specific approaches offer hope for more effective and safer treatments in the future.
引用
收藏
页码:1797 / 1806
页数:10
相关论文
共 110 条
[1]   MESANGIAL CELL APOPTOSIS - THE MAJOR MECHANISM FOR RESOLUTION OF GLOMERULAR HYPERCELLULARITY IN EXPERIMENTAL MESANGIAL PROLIFERATIVE NEPHRITIS [J].
BAKER, AJ ;
MOONEY, A ;
HUGHES, J ;
LOMBARDI, D ;
JOHNSON, RJ ;
SAVILL, J .
JOURNAL OF CLINICAL INVESTIGATION, 1994, 94 (05) :2105-2116
[2]  
BAKER PJ, 1989, AM J PATHOL, V135, P185
[3]   Management of minimal lesion glomerulonephritis: Evidence-based recommendations [J].
Bargman, JM .
KIDNEY INTERNATIONAL, 1999, 55 :S3-S16
[4]   Pathogenesis of IgA nephropathy [J].
Barratt, J ;
Feehally, J ;
Smith, AC .
SEMINARS IN NEPHROLOGY, 2004, 24 (03) :197-217
[5]  
BERGSTROM J, 1986, CLIN NEPHROL, V25, P1
[6]   TRANSFER OF EXPERIMENTAL GLOMERULONEPHRITIS IN CHICKENS BY MONONUCLEAR-CELLS [J].
BOLTON, WK ;
CHANDRA, M ;
TYSON, TM ;
KIRKPATRICK, PR ;
SADOVNIC, MJ ;
STURGILL, BC .
KIDNEY INTERNATIONAL, 1988, 34 (05) :598-610
[7]   SUPPRESSION OF EXPERIMENTAL GLOMERULONEPHRITIS BY ANTISERUM AGAINST TRANSFORMING GROWTH FACTOR-BETA-1 [J].
BORDER, WA ;
OKUDA, S ;
LANGUINO, LR ;
SPORN, MB ;
RUOSLAHTI, E .
NATURE, 1990, 346 (6282) :371-374
[8]   CONTROLLED TRIAL OF PULSE METHYLPREDNISOLONE VERSUS 2 REGIMENS OF PULSE CYCLOPHOSPHAMIDE IN SEVERE LUPUS NEPHRITIS [J].
BOUMPAS, DT ;
AUSTIN, HA ;
VAUGHN, EM ;
KLIPPEL, JH ;
STEINBERG, AD ;
YARBORO, CH ;
BALOW, JE .
LANCET, 1992, 340 (8822) :741-745
[9]   GLOMERULAR MACROPHAGES PRODUCE REACTIVE OXYGEN SPECIES IN EXPERIMENTAL GLOMERULONEPHRITIS [J].
BOYCE, NW ;
TIPPING, PG ;
HOLDSWORTH, SR .
KIDNEY INTERNATIONAL, 1989, 35 (03) :778-782
[10]   Human macrophages kill human mesangial cells by Fas-L-induced apoptosis when triggered by antibody via CD16 [J].
Boyle, JJ .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2004, 137 (03) :529-537