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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Secondary hypertension accounts for a minority of all cases of hypertension. Certain clues in the patient's medical history and laboratory parameters may help identify the rare patient with secondary hypertension. The association of hypertension with hypokalemia and renal potassium wasting should raise one's suspicion for a state of mineralocorticoid excess. The clinical syndrome of hypertension and hypokalemia may be related either to a high renin state, such as renovascular disease, or to a low renin state, such as primary hyperaldosteronism, adrenal enzyme defects, certain familial syndromes, and licorice ingestion. Over the past decade, a genetic basis has been identified for apparent mineralocorticoid excess (AME) syndrome, Liddle's syndrome, and glucocorticoid remediable aldosteronism (GRA). This brief review focuses on a few of the unusual conditions which cause a true or apparent mineralocorticoid excess state, and summarizes the clinical presentation, pathogenetic mechanism, and treatment of these diseases.
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PMID:Hypertension and hypokalemia: unusual syndromes. 906 95

Three preterm infants presented with both severe or moderate arterial hypertension and dehydration due to increased water and sodium urinary excretion. In patient 1, water and sodium wasting were extremely severe and peaked at 575 ml/kg per day and 73 mEq/kg per day, respectively. In all infants, urinary water and sodium excretion dramatically decreased when hypertension resolved. The overall clinical data suggest a pressure natriuresis phenomenon.
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PMID:Salt depletion and dehydration in hypertensive preterm infants. 909 Jun 64

Genetic defects in aldosterone biosynthesis and action affect blood pressure and electrolyte homeostasis. Aldosterone synthase deficiency, salt-wasting forms of congenital adrenal hyperplasia, and adrenal hypoplasia congenita all cause aldosterone deficiency, signs of which include hyponatremia, hyperkalemia, hypovolemia, elevated plasma renin activity, and sometimes shock and death. Conversely, the inappropriate regulation of aldosterone synthesis seen in glucocorticoid-suppressible hyperaldosteronism may cause hypokalemia, suppressed plasma renin activity, and hypertension. Similar problems occur when the normal ligand specificity of the aldosterone receptor is lost, as in the syndrome of apparent mineralocorticoid excess due to 11 beta-hydroxysteroid dehydrogenase deficiency. The effects of aldosterone are mediated largely through activation of the epithelial sodium channel, and inactivating or activating mutations of this channel leads to signs of mineralocorticoid deficiency or excess, termed pseudohypoaldosteronism and Liddle's syndrome, respectively.
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PMID:Abnormalities of aldosterone synthesis and action in children. 930 Jan 99

Persons with neuromuscular disease (NMD) have progressive weakness and wasting of skeletal muscle, reduced fat-free mass, and increased fat mass relative to healthy control subjects. To test the hypothesis that resting energy expenditure (REE), estimated total daily energy expenditure (TEE), and physical activity patterns are altered in ambulatory adults with NMD, 26 adult men and women with slowly progressive NMD and 19 able-bodied control subjects similar in age and weight were evaluated. REE was measured after an overnight fast by indirect calorimetry, TEE by heart rate monitoring, and body composition by air-displacement plethysmography. REE was not significantly different between NMD and control subjects; however, TEE was significantly reduced in NMD subjects compared with control subjects, respectively (women: 7.8 +/- 1.5 compared with 10.5 +/- 2.8; men: 10.2 +/- 3.6 compared with 12.7 +/- 2.6 MJ/d; P < or = 0.01), indicating that NMD subjects expended less energy in physical activity than did control subjects. NMD subjects also tended toward an increased energy cost of physical activity, particularly at higher activity levels (P = 0.06). Multiple regression analysis indicated that for all subjects combined, adiposity was positively associated with age and TEE and negatively associated with time spent in the active heart rate range and fat-free mass (P < or = 0.0001). This relation did not differ between NMD and control subjects, nor did it differ between men and women. We hypothesize that because of their reduced physical activity and increased adiposity, persons with NMD may be at risk for developing secondary conditions such as cardiovascular disease, hypertension, and diabetes.
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PMID:Energy expenditure, physical activity, and body composition of ambulatory adults with hereditary neuromuscular disease. 962 89

Hyponatremia is a common feature after subarachnoid hemorrhage. Hyponatremia is complex in its origin because different neuroendocrine disturbances are involved: elements of inappropriate secretion of ADH, cerebral salt wasting, and blunted response of the reninangiotensin-aldosterone system may occur simultaneously. Hyponatremia is accompanied by hypovolemia which implies a major risk for vasospasm and cerebral infarction. Hyponatremia itself might cause cerebral edema and intracranial hypertension. Fluid restriction is therefore contraindicated in hyponatremia following subarachnoid hemorrhage because of the negative impact on intravascular volume. On the contrary, replacement of both volume and sodium should be vigorously accomplished.
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PMID:[Hyponatremia in patients with subarachnoid hemorrhage]. 977 67

Despite the many technical advances in medical care and dialysis delivery, mortality and morbidity remain high in end-stage renal disease (ESRD) patients. A number of factors seem to contribute. Cardiovascular diseases are the leading cause of death: volume overload, anaemia, hypertension, arteriovenous fistula, uraemia-related myocardial cell injury all contribute to the development of ischaemic heart disease and congestive heart failure. The underlying disease is determinant for prognosis, with diabetics displaying an excess cardiovascular mortality. Elderly are also more likely to experience intercurrent medical conditions, vascular disease and diabetes, thus increasing the risk of death. Protein-energy malnutrition and wasting also contribute to the higher mortality in renal replacement therapy. Although nowadays high-risk patients are dialysed too, the rate of acceptance of ESRD patients still varies widely in different countries, possibly because of hidden selection criteria. The patients in the registries with a higher acceptance rate are more likely to be affected by co-morbid conditions and greater disease severity; the assessment of these co-morbid conditions is extremely important when comparing outcomes in different haemodialysis populations. Dialysis adequacy, obtained by means of longer duration of the treatment, is also of paramount importance; it allows minimizing the clinical effects of ultrafiltration and ensure that correct dry weight is reached. This means decreasing the incidence of intradialytic hypotensive episodes, but also improving blood pressure control, a strong predictor of survival. Family and social support, together with adequate medical care, greatly affect the quality of life of patients and can improve compliance to dialysis, diet and drugs and therefore survival.
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PMID:Morbidity and mortality on maintenance haemodialysis. 983 37

The epithelial Na+ channel (ENaC) complex is composed of three homologous subunits: alpha, beta and gamma. Mutations in ENaC subunits can increase the number of channels on the cell surface, causing a hereditary form of hypertension called Liddle's syndrome, or can decrease channel activity, causing pseudohypoaldosteronism type I, a salt-wasting disease of infancy. To investigate surface expression, we studied ENaC subunits expressed in COS-7 and HEK293 cells. Using surface biotinylation and protease sensitivity, we found that when individual ENaC subunits are expressed alone, they traffic to the cell surface. The subunits are glycosylated with high-mannose oligosaccharides, but seem to have the carbohydrate removed before they reach the cell surface. Moreover, subunits form a complex that cannot be disrupted by several non-ionic detergents. The pattern of glycosylation and detergent solubility/insolubility persists when the N-teminal and C-terminal cytoplasmic regions of ENaC are removed. With co-expression of all three ENaC subunits, the insoluble complex is the predominant species. These results show that ENaC and its family members are unique in their trafficking, biochemical characteristics and post-translational modifications.
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PMID:Cell surface expression and biosynthesis of epithelial Na+ channels. 984 84

Many factors contribute to the growth failure of chronic renal failure: water and electrolytes disturbances, hypertonicity, phosphate or calcium wasting, secondary hyperparathyroidism, anemia, hypertension, metabolic acidosis, and malnutrition. In addition, the pubertal growth spurt is usually stunted. Growth hormone (GH) resistance is observed with low GH binding protein (GHBP) level, and normal or low IGF I levels despite elevated GH level. Elevated IGFBP levels may contribute to a reduced IGF activity, especially in dialysed patients. Glucocorticoid therapy in transplanted patients further contribute to poor growth and inhibited IGF I activity. As conventional treatments have a limited effect to improve growth, adult height is often far below -2 SD. GH therapy has proved to be successful, especially in young children, overpassing the hormonal resistance so that an adult height within the normal range may be reached.
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PMID:[Physiopathology of the somatotropin axis in chronic renal insufficiency]. 985 82

Recommendations for endpoints in clinical trials of wasting that involve exercise should involve selection that clearly identifies the effects of exercise. Broad endpoints such as morbidity and mortality must be corrected for the effects of age, smoking, hypertension, etc. in order to gain adjusted information pertinent to exercise. Selection of variables related to physiological function although more specific i.e., maximal oxygen uptake, must still be viewed from the perspective that other variables may contribute to the values measured. Nevertheless, physiological information obtained from performance tests may well provide useful endpoints. In this regard, V02 max, heartrate and pulmonary ventilation at fixed work loads, muscular strength, reaction time, flexibility, blood gases, cardiac output, stroke volume, serum lactate, and properties of skeletal muscle such as mitochondria concentration and components related to muscle energetics, e.g., adenosine triphosphate. In addition exercise will definitely impact body mass and composition as well as configuration. The latter is assessable through utilization of somatogramography. Analysis of muscle depends on muscle biopsy and magnetic resonance spectroscopy. Neither of these methods has been employed in clinical trials to the best of our knowledge. Thus, one needs evidence that exercise in the clinical trial provides a discrete effect on performance capabilities, body status and biologically important variables.
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PMID:Perspectives on exercise and wasting. 991 18

The epithelial Na+ channel (ENaC) controls the rate-limiting step in the process of transepithelial Na+ reabsorption in the distal nephron, the distal colon, and the airways. Hereditary salt-losing syndromes have been ascribed to loss of function mutations in the alpha-, beta-, or gamma-ENaC subunit genes, whereas gain of function mutations (located in the COOH terminus of the beta- or gamma-subunit) result in hypertension due to Na+ retention (Liddle's syndrome). In mice, gene-targeting experiments have shown that, in addition to the kidney salt-wasting phenotype, ENaC was essential for lung fluid clearance in newborn mice. Disruption of the alpha-subunit resulted in a complete abolition of ENaC-mediated Na+ transport, whereas knockout of the beta- or gamma-subunit had only minor effects on fluid clearance in lung. Disruption of each of the three subunits resulted in a salt-wasting syndrome similar to that observed in humans.
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PMID:Genetic disorders of membrane transport. V. The epithelial sodium channel and its implication in human diseases. 1007 30


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