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Query: UMLS:C0035078 (renal failure)
31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension or high blood pressure is a risk factor that increases risk of myocardial infarction, renal failure or cerebral stroke. The pathogenesis of hypertension is due to a variety of causes, including inherited predisposition, dietary habits, especially salt intake, smoking, and also 'general lifestyle'. But for the scientist interested in the complex interplay of physiological and molecular factors, the actual causes of high blood pressure remain uninvestigated. The following article is concerned with new reports that ouabain, a plant derivative, occurs in human beings, in whom it appears to have a hormonal function; ouabain may even play a key role in the pathogenesis of hypertension. We are thus brought a step closer to the background of cardiovascular disease; we may also be afforded a lead to a new therapeutic principle.
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PMID:Ouabain--a link in the genesis of high blood pressure? 147 73

Elevated blood pressure (BP) is of special clinical significance because of its association with pathophysiologies such as heart disease, renal failure, and stroke. We described the development of a protocol for use with hypertensive rats in which prepubertal exposure to a high salt (8% NaCl) diet results in a pathophysiological syndrome including rapid increase in BP, failure to maintain normal weight gain, renal damage, cerebrovascular lesions, and early mortality. These phenomena are described for the inbred spontaneously hypertensive rat (SHR), and for reciprocal F1 hybrids of a cross between SHR and the Dahl salt-sensitive (SS/Jr) inbred strain. The study with reciprocal F1s revealed striking effects of maternal environment on pathophysiological response to a high salt diet. F1s nurtured by SHR mothers weighed less at 35 days of age, and after exposure to the high salt diet suffered more rapid BP increases, greater incidence of stroke, body weight loss, and mortality, than F1s nurtured by SS/Jr dams. These results suggest that maternal mediation of the nutritional status of the animal may play an important role in determining susceptibility to elevated BP and subsequent pathophysiology associated with exposure to a high salt diet. The implication of these findings for human hypertension is briefly discussed.
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PMID:Maternal influences on cardiovascular pathophysiology. 153 41

To test the hypothesis that restriction of sodium intake during the first 3 to 5 days of life will prevent the occurrence of hypernatremia and the need for administration of large fluid volumes, we prospectively and randomly assigned 17 babies (mean +/- SD: 850 +/- 120 gm; 27 +/- 1 weeks of gestation) to receive in blind fashion either daily maintenance sodium or salt restriction with physician-prescribed parenteral fluid intake. Maintenance-group infants received 3 to 4 mEq of sodium per kilogram per day; restricted infants received no sodium supplement other than with such treatments as transfusion. Sodium balance studies conducted for 5 days demonstrated that maintenance salt intake resulted in a daily sodium balance near zero, whereas sodium-restricted infants continued to excrete urinary sodium at a high rate, which promoted a more negative balance (average daily sodium balance -0.30 +/- 1.78 SD in maintenance group vs -3.71 +/- 1.47 mEq/kg per day in restriction group; p less than 0.001). Care givers tended to prescribe daily increases in parenteral fluids for the salt-supplemented infants, perhaps because serum sodium concentrations were elevated in these infants after the first day of the study (p less than 0.001). Hypernatremia developed in two sodium-supplemented infants (greater than 150 mEq/L), and hyponatremia developed in two sodium-restricted infants (less than 130 mEq/L); however, the restricted infants were more likely to have normal serum osmolality (p less than 0.05). Both groups of infants produced urine that was neither concentrated nor dilute, with a high fractional excretion of sodium; renal failure was not observed. The mortality rate was not affected, but the incidence of bronchopulmonary dysplasia was significantly less in the sodium-restricted babies (p less than 0.02). We conclude that in tiny premature infants, a fluid regimen that restricts sodium may simplify parenteral fluid therapy targeted to prevent hypernatremia and excessive administration of parenteral fluids.
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PMID:Sodium restriction versus daily maintenance replacement in very low birth weight premature neonates: a randomized, blind therapeutic trial. 140 8

Since amphotericin B nephrotoxicity is mediated, in part by hypoxic tubular injury, the role of endothelin in the renal vasoconstriction, characteristic of amphotericin toxicity has been studied. Intact and salt depleted rats were infused with amphotericin B (20 micrograms/kg per min) or 5% dextrose over 20 min. Plasma endothelin levels determined at the conclusion of the infusion period, did not differ between the experimental groups, despite a marked reduction in renal blood flow noted in rats infused with amphotericin B. Amphotericin B (10(-5)-10(-7) M) did not stimulate endothelin release from cultured bovine aortic endothelial cells. However, in a model of chronic amphotericin nephrotoxicity produced by repeated daily intraperitoneal injections of amphotericin B (5 mg/kg) to salt depleted rats, renal failure was associated with elevated plasma endothelin levels (29.3 +/- 4.4 fmol/mL, vs 10.8 +/- 1.2 fmol/mL in salt depleted controls, P less than 0.01). We conclude that while plasma endothelin may be increased in chronic amphotericin B nephropathy, this peptide does not mediate the acute renal vasoconstriction associated with the infusion of this drug.
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PMID:In-vivo and in-vitro studies on the effect of amphotericin B on endothelin release. 173 26

African-Americans with essential hypertension are more prone to the development of renal failure and are frequently salt-sensitive as well. Because alterations of intrarenal hemodynamics are important in the progression of renal disease and because salt-sensitive animal models with hypertension manifest a greater propensity to develop glomerulosclerosis in association with a rise in glomerular capillary pressure, we tested whether the renal hemodynamic adaptation to high dietary Na+ intake differs in salt-sensitive and salt-resistant hypertensive patients. We studied 17 black and nine white patients with essential hypertension who were placed on a low Na+ diet (20 meq/day) for 9 days, followed by a high Na+ diet (200 meq/day) for 14 days. During the last 4 days of each diet regimen, they received 30 mg/day of slow-release nifedipine. Eleven blacks were salt-sensitive, and all whites were salt-resistant. During the low Na+ diet period, salt-sensitive and salt-resistant patients had similar mean arterial pressure, glomerular filtration rate, effective renal plasma flow, and filtration fraction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal renal hemodynamics in black salt-sensitive patients with hypertension. 174 61

Atrial natriuretic peptide has been considered to be a major regulator in the body's water and salt homeostasis. Antagonizing those mechanisms leading to volume retention and overload (renin, angiotensin, aldosterone), ANP has been suggested to play a critical role in the pathology of certain diseases like renal failure, congestive heart failure or hypertension. In this regard, we measured ANP plasma concentration in normal healthy dogs and dogs with renal failure, congestive heart failure and Cushing syndrome. ANP levels were slightly decreased in dogs with Cushing disease (n = 9; 5.5 +/- 2 fmol/ml), increased in renal failure (n = 7; 16.2 +/- 5.8 fmol/ml, p less than 0.05) and markedly augmented in dogs with congestive heart failure (n = 14; 52.9 +/- 29.75 fmol/ml, p less than 0.01) as compared to healthy dogs (n = 6; 8.3 +/- 3.5 fmol/ml). Furthermore, characterization of the measured immunoreactivity (IR-ANP) revealed, that up to 50% of the IR-ANP in dogs with congestive heart failure corresponds to the ANP precursor molecule, not found in healthy subjects. This fact might present one possible explanation for the attenuated response to ANP in congestive heart failure. In addition, this finding may also serve a diagnostical purpose.
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PMID:[Diagnostic possibilities of ANP blood measurements in dogs]. 182 66

Lithium therapy can induce acute toxic reactions especially during overdosage. Exceptionally, permanent neurologic sequelae persist after the acute toxic reaction. These sequelae are more often cerebellar symptoms. Dementia, parkinsonian syndromes, choreoathetosis, brain stem syndromes and peripheral neuropathies have also been described. They are defined as irreversible if they persist more than two months after the interruption of lithium treatment. These neurologic complications occur frequently after voluntary or accidental poisoning but they may be observed even if the serum lithium dosage is below toxic level. Risk factors other than overdose are not well identified. Neurologic lesions induced by lithium can occur in the first days of the treatment as well as after years of maintenance therapy. Age and psychiatric diagnosis do not seem to be correlated with an increased risk of lithium induced neurotoxicity. Sex may be a risk factor, because of an overrepresentation of women among the case reports. The lithium-neuroleptic combination is another possible (although controversial) risk factor precipitating the occurrence of irreversible neurologic sequelae. Haloperidol was first implicated, but it has been shown that others neuroleptics, in combination with lithium, can induce similar toxic reactions. Intercurrent somatic illness with pyrexia often precedes the acute toxic reaction, and special attention must be paid to patients treated by lithium when they become hyperthermic. Major surgery, concurrent treatment with diuretics, renal failure, low food intake or low-salt diet are more uncommon precipitating factors. Available pharmacological treatments have not yet proved to be helpful. Even when the lesions are irreversible, a functional improvement can be obtained by rehabilitation. Thirty one cases of irreversible neurologic sequelae are reviewed.
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PMID:[Irreversible neurologic sequelae caused by lithium]. 186 56

The prevalence of hypertension increases with age. The majority of the hypertensive population is over age 55. Although the treatment of systolic hypertension remains incompletely understood, the reduction of diastolic hypertension with pharmacotherapy has been shown to reduce complications from hypertension in persons over age 55. The older hypertensive patient is at risk for the same complications as the younger patient: angina, myocardial infarction, arteriosclerosis obliterans, stroke, myocardial hypertrophy, congestive heart failure, and renal failure; the risk of sudden death and multi-infarct dementia in the older patient may be somewhat higher. The older hypertensive individual may have reduced plasma volume and defective salt and water conservation, reduced renal function, impairment of baroreceptor reflexes and sympathetic reactivity, and altered drug pharmacokinetics, or may have arteriosclerosis leading to pseudohypertension. Many circumstances interfere with adequate compliance with therapeutic regimens among the elderly. Concomitant medical conditions increase the possibility of drug interactions and require that the practitioner be able to adjust the antihypertensive program to the patient.
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PMID:Treatment considerations for the hypertensive patient over age 55. 189 46

We previously reported that long-term omega-3 fatty acid deficiency is associated with increased water intake in rhesus monkeys. To determine whether the increase was specific to water, intakes of salt solutions were measured in 15-minute single-bottle tests. Deficient monkeys drank at least twice as much of all NaCl concentrations as controls. Overall intake decreased as salt concentration increased. In 2-bottle preference tests, deficient monkeys again drank more total fluid but neither preferred nor avoided normal saline compared to controls. When deprived of water, deficient monkeys concentrated urine as well as controls, demonstrating that the increased intake was not a result of renal failure or diabetes insipidus. Omega-3 fatty acids have roles both in neural membrane function and in metabolism of prostaglandins and other eicosanoids. Omega-3 fatty acid deficiency may affect drinking through changes in one or both of these functions.
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PMID:Increased intake of water and NaCl solutions in omega-3 fatty acid deficient monkeys. 189 94

Three dietary measures are useful for chronic progressive renal failure. In a hypertensive patient, salt restriction is a prerequisite for antihypertensive therapy. Protein restriction to 0.6 g/kg of body weight per day can slow down progression of renal disease with the exception of polycystic disease of the adult type. Ketosteril can be given for prevention of essential amino acid deficiency. A normalization of serum phosphorus is essential for slowing progression of disease as well as bone metabolism. Therefore, a diet reduced in phosphates, supported by phosphate binders is prescribed.
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PMID:[Nutrition in kidney diseases]. 192 35


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