ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Glomerular diseases are associated with changes in glomerular membrane permeability properties that alter filtration rate of plasma water and barrier function of the capillary wall. To estimate intrinsic permeability properties that regulate trasmembrane transport of water and macromolecules, theoretical analysis of renal clearance of tracer molecules can be used. The development of adequate theoretical models is required to achieve sufficient accuracy to simulate complicated biological processes. Current research in this area is aimed at improving and validating the presently available models in order to characterize the nature of permeability changes associated with pathological conditions. This is a key step in understanding the pathophysiological nature of glomerular diseases and in the development of effective treatments.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The sensitivity of the renal vasculature to endothelin-1 together with the effect of the peptide on the kidney prompted investigators to study the role of endothelin-1 in renal pathophysiology. The kidney expresses both endothelinAand endothelinBreceptors, which differ from species to species. Experiments employing specific endothelin receptor antagonists in experimental animals have suggested a role for endothelin-1 in ischaemia-induced acute renal failure and renal disease progression.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The fundamental role of cell-mediated immunity in inflammatory disease of the kidney has been established for some time. This review focusses on the recent advances in our understanding of the role of T-cells in the pathogenesis both of glomerulonephritis and interstitial nephritis. In particular, the increasing experimental evidence for a functional role for T-cell in promoting disease intiation and progression is examined. The ever increasing variety T-cell-effector functions and their relevance are also discussed.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Nitric oxide has fundamental roles in the modulation of many cell functions. In glomerulonephritis, generation of nitric oxide by the acutely inflamed glomerulus has recently been confirmed, with evidence that synthesis occurs through induction of the inducible form of nitric oxide synthase. Recent studies implicate infiltrating macrophages as a major source of this activity, although intrinsic glomerular cells may contribute as nitric oxide synthase has been found in cytokine-stimulated mesangial, endothelial and epithelial cells in culture. Cytokines, which are known to have a central role in glomerulonephritis, are the most probable stimulus of nitric oxide synthase inductionIn vivo,although this awaits confimation. A role for nitric oxide in the pathophysiology of glomerulonephritis is not clearly defined at present but is strongly suggested by evidence for paticipation of nitric oxide in other immune and inflammatory diseases. The evidence evaluated in this review emphasizes that the role is certain to be complex. As yet it is not possible to predict whether the modulatory effects of nitric oxide on glomerular haemodynamics, vascular integrity, leucocyte infiltration and intrinsic glomerular cell responses are predominantly protective or cytotoxic. There are presently only two fully published reports of inhibition of nitric oxide in models of glomerulonephritis, one of which showed an exacerbation of acute heterologous nephrotoxic injury, and the other showed amelioration of chronic autoimmune glomerulonephritis. It is therefore premature to speculate on the effects of nitric oxide inhibition in glomerulonephritis. New insights await further understanding of the regulation of the inducible form of nitric oxide synthase in glomerulonephritis and the availability of specific inhibitors of this enzyme.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Recent evidence suggests that decreased degradation of the glomerular extracellular matrix may contribute to the matrix accumulation that occurs in the progression of chronic renal disease. The presence of matrix metalloproteinases in cultured glomerular cells and possibly in glomeruliin vivocombined with the ability of these proteinases to degrade extracellular matrix components suggests that these proteinases may play important roles in glomerular extracellular matrix degradation. Decreased activity of these proteinases mediated by upregulation of their inhibitors could theoretically contribute to matrix accumulation. In the limited number of studies that have addressed this issue directly, there is evidence both to support and refute this hypothesis. It is reasonable to suspect, however, that either increased matrix formation, decreased matrix degradation, or both, might contribute to extracellular matrix accumulation in progressive renal disease, depending on the primary etiology.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Proteinuria may be an independent risk factor for nephroscierosis. One potential mechanism has emerged with the finding that lipoproteins, including albumin, modulate the biology of mesangial cells and proximal tubular epithelial cells when internalized. Consequent alterations in renal-cell lipid metabolism may underlie some of these effects.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Remarkable progress has been made in the past two years in the investigation of immunological events and effector mechanisms which lead to glomerular inflammation and tissue damage, suggesting a number of areas in which therapeutic modulation is possible. We review recent advances in the two major areas of investigation in this field: the nephritogenic response to glomerulonephritis and local inflammatory reaction, and the novel therapeutic perpectives that have emerged from insights into the biology and pathology of the immune and inflammatory response.

ISSN:1062-4821    

出版商:OVID    

年代:1995

数据来源: OVID