ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The molecular basis of the organogenesis of the mammalian kidney is being investigated at multiple levels, with several exciting developments. Cellular signaling during and after kidney induction may be mediated in part by Wnt genes, which encode secreted, matrix-associated peptides. The Wilms' tumor suppressor gene WT1 is required for the kidney mesenchyme to respond to induction; the transcription factor Pax-2 may regulate the aggregation and proliferation of the kidney mesenchyme immediately after induction. Although the links between signaling molecules, their receptors, and the activation and repression of transcription factors in the kidney remain to be determined, several key elements of the genetic cascade driving kidney morphogenesis are now characterized.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

In animal models of acute renal injury, administration of epidermal, insulin-like or hepatocyte growth factor accelerates restoration of kidney function and normalization of histology, and reduces mortality. Mechanisms for such action include stimulation of anabolism, maintenance of glomerular filtration, and enhancement of tubular regeneration. Further studies are needed to establish the utility of growth factors as therapeutic agents for acute renal failure in humans.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Apoptosis or programmed cell death is a major focus of interest in many fields of research. Recent advances include definition of key molecules driving the cell death programme, including Fas and Fas-ligand in the plasma membrane, and cytoplasmic proteases such as interleukin-1β-converting enzyme. These are kept in check by 'survival' signals conferred by exogenous cytokines and the extracellular matrix, or by endogenous proteins encoded by the bcl-2 gene family. Important insights into the programme of mammalian cell death have come from comparative biology. The scene is now set for study of apoptosis in renal health and disease, in which recent studies indicate key roles in remodelling of both glomeruli and tubules after renal injury.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Advances in basic immunology have markedly enhanced our understanding of immune-mediated renal disease, particularly in view of the growing recognition of the importance of T-cells in mediating renal injury. Recent milestones in investigative technology, including cell-culture techniques supporting T-cell clones and renal-derived cell populations, and genetic inbreeding of both recombinant and transgenic mice, provide a unique opportunity to study specific mechanisms of cell-mediated responses that target the kidney. In the past year the role of major histocompatibility complex molecule expression and T-cell repertoire selection has been better defined in some models of autoimmune renal disease. In addition, new observations regarding mechanisms that down regulate injurious T-cell-mediated responses may direct further studies that develop new therapeutic modalities.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Endothelial activation is central to the pathophysiology of glomerulonephritis, vasculitis, allograft rejection, ischemia-reperfusion injury and thrombotic angiopathies. Major advances in endothelial biology during the past year have emphasized the importance of selectin, mucin, integrin, and immunoglobulin-like adhesion molecules in leukocyte trafficking in glomerular inflammation, and have defined novel mechanisms by which leukocyte-endothelial cell interactions are regulated by inflammatory mediators and cytokines. These breakthroughs have already spawned experimental immunosuppressive strategies that should antecede the development of novel, potent and specific therapies for common renal diseases.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Hepatitis C virus (HCV) infection is a major cause of chronic liver disease and is associated with a variety of extrahepatic manifestations, including cryoglobulinemia and glomerulonephritis. Epidemiologic evidence suggests that HCV infection may be a major risk factor for both cryoglobulinemic and type I membranoproliferative glomerulonephritis (MPGN). Clinical symptoms and laboratory data may or may not reflect the presence of chronic liver disease. Most patients have evidence of hypocomplementemia, circulating rheumatoid factors, and cryoglobulinemia. The pathogenesis of HCV-associated MPGN is probably a result of glomerular deposition of circulating HCV and anti-HCV antibodies. Treatment with interferon-cc has been shown to improve proteinuria, suppress viremia, and stabilize renal function. However, patients often relapse after therapy is stopped. The optimal therapy remains to be defined but may involve different dosage regimens of interferon-a or the combination of several antiviral agents.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID