ISSN:1062-4821    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The endothelin system has been implicated in the pathogenesis of arterial hypertension and renal disorders. Endothelin-1, the predominant isoform of the endothelin peptide family, regulates vasoconstriction and cell proliferation in tissues both within and outside the cardiovascular system through activation of Gi-protein-coupled ETAand ETBreceptors. Endothelin synthesis is regulated through autocrine mechanisms by endothelin converting enzymes, chymases, and non-endothelin converting enzyme metalloproteases. In-vitro experiments have demonstrated that endothelin-1 stimulates growth in vascular smooth muscle and in the kidney. Recent studies indicate that endothelin mRNA and protein are also increasedin vivoin the kidney and vasculature in hypertension and renal disease. Studies using molecular or pharmacological inhibition of the endothelin system demonstrate that endothelin-1 contributes to the functional and structural changes associated with arterial hypertension and glomerulosclerosis, and that these effects are only in part dependent on blood pressure. These experimental studies and first clinical trials suggest that endothelin antagonists may offer therapeutic potential to reduce end-organ damage in diseases associated with vascular remodeling and renal injury.

ISSN:1062-4821    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Interest has blossomed in the development of complement inhibitors, in parallel with a growth in our understanding of the biology of the complement cascade. The first generation of designed inhibitors was based on naturally occurring complement receptors and regulatory molecules. These agents provided useful tools for exploring the role of complement in experimental models of disease, but may have limited therapeutic application in humans because of their short half-lives, limited bioavailability and possible antigenicity. More recently, humanized antibodies and synthetic molecules that block the activation of complement have been developed, which look as though they may overcome some of these difficulties. The possibility for precision inhibition of a limited part of the complement cascade, or for inhibition confined to a single organ, may offer effective therapeutic results, while avoiding the disadvantages of nonselective complement blockade. This review examines the recent evidence that complement inhibition will reduce tissue damage resulting from organ transplantation, ischaemia-reperfusion injury, cancer, glomerulonephritis and the use of extracorporeal circuits.

ISSN:1062-4821    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The immunosuppressive drug mycophenolate mofetil is a potential new treatment for autoimmune renal disease. In addition to its effects in modulating the autoimmune response, mycophenolate mofetil reduces adhesion molecule expression and delays the progression of renal failure. Data from experimental models of glomerulonephritis, especially of lupus nephritis, have demonstrated that mycophenolate mofetil reverses both inflammatory and autoimmune aspects of disease and influences outcome. As yet, clinical experience with mycophenolate mofetil remains anecdotal but provides a strong platform for the scientific evaluation of mycophenolate mofetil as a new therapeutic agent for these conditions in the future.

ISSN:1062-4821    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Vascular access dysfunction continues to result in substantial morbidity for chronic hemodialysis patients. Pharmacologic and molecular biologic approaches to prevention of vascular access dysfunction, if clinically successful, will be cost effective and improve quality of life for chronic dialysis patients. This review summarizes currently available information and future prospects in pharmacologic and molecular biologic approaches to preventing vascular access stenosis.

ISSN:1062-4821    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The target hematocrit to be achieved when treating anemia in hemodialysis patients with erythropoietin is controversial. Current evidence-based recommendations suggest a target hematocrit range of 33% to 36%. Small studies suggest that normalization of hematocrit with erythropoietin may benefit hemodialysis patients in terms of brain function, physical performance, quality of life, and prevention of progressive left ventricular dilatation. However a recent study of the effects of erythropoietin-induced normalization of hematocrit in hemodialysis patients with symptomatic heart disease has shown an increase in both mortality and the rate of vascular access thrombosis. Currently, normalization of hematocrit in patients with symptomatic heart disease is not recommended, nor is it possible to conclude that possible benefits of normalization of hematocrit will outweigh risks in hemodialysis patients without symptomatic heart disease.

ISSN:1062-4821    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The development of transgenic mice carrying the simian virus-40 large T antigen gene or the temperature-sensitive simian virus-40 large T antigen gene, either alone or placed under the control of the 5′-regulatory regions of tissue-specific or ubiquitous genes, has permitted the production of differentiated, polarized kidney epithelial cells. This review covers the immortalized cell lines issued from the various parts of the renal tubule and, in particular, the recently established collecting duct cell lines that have been used as ex-vivo cell models to analyze the regulation of ion transport processes by hormones.

ISSN:1062-4821    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Recent discoveries of calcium-regulating and calcium-transporting proteins have paved the way for a heightened understanding of the mechanisms and control of renal calcium transport. In this review, new findings regarding the multifunctional megalin receptor, chloride channels, a putative calcium entry channel, and the calcium-sensing receptor are discussed.

ISSN:1062-4821    

出版商:OVID    

年代:1999

数据来源: OVID