ISSN:1062-4821    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

The branching of the ureteric bud and the differentiation of renal mesenchyme into nephrons are interdependent processes. Experiments with organ culture and genetically engineered mice suggest that metanephric growth factors regulate these events. Renal mesenchyme produces glial cell line-derived neurotrophic factor, an essential molecule for ureteric bud growth, whereas multiple growth factors are required for nephron formation: these include fibroblast growth factor 2, Wnt4 and bone morphogenetic protein 7. Deregulation of growth factors may be implicated in the pathogenesis of congenital kidney malformations.

ISSN:1062-4821    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

X-linked hypophosphatemia is a heritable form of rickets characterized biochemically by phosphaturia and abnormal bioactivation of vitamin D. Recent advances include the observation, using kidney cells from the X-linked hypophosphatemia mouse model (Hyp), that in-vitro renal phosphate transport is normal yet bone mineralization may be intrinsically abnormal. Of special interest is the identification of a gene (PEX) that is mutated in X-linked hypophosphatemic patients.

ISSN:1062-4821    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

The proximal tubule in the kidney is a main organ for the metabolic clearance of small peptide hormone, and is intensively involved in reabsorption, storage and homeostatic regulation of different vitamins. Recently,the endocytic membrane protein megalin has been shown to bind several smaller peptides, including insulin and epidermal growth factor, as well as to bind and mediate uptake of transcobalamin-B12, attracting new attention on the cellular mechanisms involved in these processes.

ISSN:1062-4821    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Angiotensin (Ang) II is not the only active peptide of the renin-angiotensin system. Several of its degradation products including Ang III (obtained by deletion of the N terminal amino acid), Ang IV (obtained by deletion of the two N terminal amino acids) and Ang ll(1-7)(obtained by deletion of the C terminal amino acid) also possess biological functions. These peptides are formed via the activity of several enzymes, aminopeptidase A for Ang III, aminopeptidases A and N for Ang IV, prolylendopeptidase and carboxypeptidases for Ang ll(1-7). Ang III possesses most of the properties of Ang II and shares the same receptors. This peptide is particularly important in brain and pituitary physiology and plays a major role in the secretion of arginine vasopressin. Ang IV possesses its own receptors distinct from AT1and AT2. Some of its effects (for example, stimulation of the synthesis of the type 1 inhibitor of plasminogen activator by endothelial cells) were previously attributed to Ang II. Others are opposed to Ang II effects (renal and cerebral vasodilation). Its role in vascular, renal and cerebral physiology remains to be determined. Ang 11(1-7)exhibits direct and indirect effects, the latter resulting from Ang ll(1-7)-dependent formation of nitric oxide and vasodilatory prostaglandins. Ang ll(1-7)recognizes both specific receptors and ATi receptors as shown by the partial antagonistic properties of losartan. Ang ll(1-7)plays essentially a role in the control of the hydroelectrolytic balance by increasing glomerular filtration rate, urinary output and sodium excretion rate

ISSN:1062-4821    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Sodium homeostasis is crucial for the control of extracellular volume and blood pressure. Regulation of sodium reabsorption is mainly achieved in the distal nephron by the mineralocorticoid aldosterone, but the molecular pathway of aldosterone action has largely remained unclear.Molecule genetic analysis of inherited diseases distribution sodium homeostasis has now demonstrated that the amiloride-sensitive epithelial sodium channel is a major effector of aldosterone action. Mechanisms by which aldosterone regulates the epithelial sodium channel activity are beginning to emerge and will be of great importance for a better understanding of salt-sensitive hypertension.

ISSN:1062-4821    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

In recent years, considerable progress has been made in our understanding of the pathophysiology of secondary hyperparathyroidism in chronic renal failure and the contribution of the level of circulating parathyroid hormone to the genesis of the various types of uremic bone disease. A better insight into the cellular and molecular basis of abnormal parathyroid hormone secretion has been obtained; in particular the abnormal expression of the receptors for calcium and vitamin D in the hyperplastic parathyroid tissue, the demonstration of a direct enhancing effect of extracellular phosphate on parathyroid hormone secretion, the involvement of abnormally expressed growth factors such as transforming growth factor-a in parathyroid hyperplasia, and the occurrence of monoclonal parathyroid cell growth, which is probably responsible for the eventual development of autonomous hyperparathyroidism. In the pathogenesis of osteitis fibrosa, a synergistic action of parathyroid hormone with cytokines and growth factors is highly probable from a theoretical point of view, and personal preliminary observations support this hypothesis. The relative importance of metabolic acidosis is controversial. The existence of a skeletal resistance to parathyroid hormone in chronic renal failure could be partly as a result of a down-regulation of the parathyroid hormone/parathyroid hormone-related peptide receptor. In the presence of normal or only slightly elevated plasma intact parathyroid hormone levels, this may favour the development of adynamic bone disease. Finally, in terms of clinical practice the non-invasive diagnosis of the precise type of renal osteodystrophy will require the introduction of recently developed, more accurate plasma markers of bone formation and resorption, in addition to plasma intact parathyroid hormone.

ISSN:1062-4821    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:1062-4821    

出版商:OVID    

年代:1997

数据来源: OVID