摘要:

Little information is available about either the potential beneficial or harmful effects of estrogen replacement therapy in postmenopausal women with end-stage renal disease. Although evidence supports a role for estrogen replacement therapy in postmenopausal women in the prevention of cardiovascular disease and bone loss, possible improvement in cognitive function, and the relief of menopausal symptoms, these conclusions may not be applicable to patients with end-stage renal disease, since these studies have generally excluded such women. This issue is of considerable importance since cardiovascular causes account for more than 50% of the all-cause mortality in patients with end-stage renal disease. However, estrogen replacement therapy may also have untoward effects in patients with the disease, including an increased risk of dialysis access thrombosis and potentially worsening coronary artery disease in postmenopausal patients. Furthermore, dosing of estrogens needs to be done carefully since renal excretion is important for the elimination of estrogen metabolites. Low dose or alternate day dosing in addition to monitoring estrogen levels may be warranted when prescribing estrogen replacement therapy to women with end-stage renal disease. In this review, it is our objective to analyze the evidence published in the literature so far and to weigh the risks and benefits of estrogen therapy in postmenopausal women with end-stage renal disease.

ISSN:1062-4821    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Growth factor production, glomerular cell proliferation and glomerular extracellular matrix expansion are prominent features of mesangioproliferative and crescentic glomerulonephritides. Recent studies have provided additional insights into the mechanisms of mesangial cell proliferation and interaction with extracellular matrix, and have focused on selective interruption of relevant mediators of injury. Studies into mitogenic signalling and cell cycle regulation in glomerular epithelial cells support a pathogenetic role for growth factors and glomerular epithelial cell proliferation in focal segmental glomerulosclerosis, and possibly membranous nephropathy. A better appreciation of growth factor pathways may lead to new treatment strategies for human glomerulopathies.

ISSN:1062-4821    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Chemokines have been verified as inflammatory mediators of experimental nephritis by using anti-chemokine antibodies, chemokine receptor antagonists or targeted chemokine gene disruption. In human disease, chemokines are expressed in the kidney in association with inflammatory infiltrates. Chemokine blockade is thus a potentially novel approach to therapy of inflammatory renal disease. Several anti-chemokine strategies are under development. Effective use of anti-chemokine therapy for renal disease will require a precise understanding of the unique roles that individual chemokines have in renal pathology, and the genetic factors that regulate chemokine expression.

ISSN:1062-4821    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Many peptides influence renal function and structure in physiological and pathophysiological situations. Bioactive peptides that regulate renal function and structure encompass various substances including vasopeptides, growth factors, cytokines and peptide hormones. We highlight some novel concepts indicating that the vasoactive peptides angiotensin II and endothelin-1 play a major role in the progression of renal disease. These effects may be amplified by reduced concentration of counteracting natriuretic peptides. In addition, recent evidence suggests that peptides such as leptin, previously not considered to exert any renal effects, may be involved in renal pathophysiology under certain conditions. One of the most imperative tasks in nephrology is to develop innovative strategies to slow the progression of chronic renal disease. Interference with the renal action of bioactive peptides will certainly be part of this strategy.

ISSN:1062-4821    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

The role of cell cycle regulatory proteins in progression is elucidated. Human renal biopsy data show amelioration and even regression of structural injury with interventions. Data implicate new mechanisms of the renin-aldosterone-angiotensin system in progressive injuries, including immune modulation and a direct effect of aldosterone on progression. New approaches and interventions that target these fibrotic responses show promising results.

ISSN:1062-4821    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Branching morphogenesis, mesenchymal cell condensation and mesenchymal-to-epithelial conversion are key steps in kidney development and morphogenesis of several other organs. Review articles describing our current knowledge of the genetic and molecular regulation of these processes have been published. Therefore, this review focuses on the important question of cell lineage specification during kidney development. We describe how new insights are being made into the specification of kidney cells in the intermediate mesoderm, as well as specification of cells that will form the renal mesenchyme, ureteric duct, nephron tubule epithelium and renal vasculature.

ISSN:1062-4821    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

At the forefront of the revolution in human genomics is DNA microarray technology, which evaluates expression levels or genotypes of thousands of genes simultaneously, by means of miniaturization and parallel processing. Furthermore, advances in bioinformatics will result in the creation of large databases, which will require complex software programming for structural analysis. Over the next decade, DNA microarrays, combined with sophisticated informatics and genomic databases, will provide molecular fingerprints of disease processes and prognoses. This review provides an update on DNA microarray technology and its application to renal diseases.

ISSN:1062-4821    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

The year 1999 saw considerable activity in the area of hypertension-related molecular genetics. Several new monogenic hypertensive disorders, as well as a monogenic form of hypotension, were elucidated. Molecular genetics has made significant inroads in explaining basic mechanisms of magnesium homeostasis. Linkage strategies have been applied in family studies, sib-pair analyses, and twin studies. More stringent criteria for association studies have been formulated. The 11 β-hydroxysteroid dehydrogenase gene, the prostacyclin synthase gene, genes coding for variants in G proteins, and adrenergic receptor genes have received particular attention. On the horizon are better phenotyped patient and subject collectives, expanded genotyping with the availability of a 300 000 genome-wide single-nucleotide polymorphism map, multigenic studies in the form of metabolic control analyses, and new bioinformatic strategies including neural networks.

ISSN:1062-4821    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Recently published observational epidemiologic studies and clinical trials have provided additional evidence that weight loss, dietary sodium reduction, moderation of alcohol consumption, physical activity, and potassium supplementation reduce blood pressure. Lifestyle modification should be recommended for the prevention and treatment of hypertension in the general population.

ISSN:1062-4821    

出版商:OVID    

年代:2000

数据来源: OVID