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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between young maternal age and preterm delivery was investigated in a subsample of 605 primigravidas enrolled in the Camden (New Jersey, US) Study. Included were 366 adolescents under 16 years of age (cases) and 239 women 18-29 years of age (controls). 36.3% of young mothers had a low gynecological age (i.e., their chronological age was 2 or fewer years more than their age at menarche). After adjustment for ethnicity, cigarette smoking, weight gain rate, height, fetal sex, gestational diabetes mellitus, and pregnancy-induced hypertension, the odds ratio (OR) of preterm labor among young adolescents was 1.74 (95% confidence interval (CI), 1.07-2.84) and that of preterm delivery was 2.08 (95% CI, 1.08-4.00). There was a modest decreased risk of preterm delivery attributable to other causes (e.g., premature rupture of the membranes) among the youngest women (OR, 0.70; 95% CI, 0.28-1.75). Young age with low gynecological age was associated with a 2.15 OR (95% CI, 1.19-3.89) of preterm labor and a 2.64 OR (95% CI, 1.23-5.65) of preterm delivery with preterm labor. The risk associated with young age and higher gynecological age was increased only moderately. These findings suggest that it is the biological immaturity often associated with young age, rather than young maternal age per se, that increases the risks of adolescent pregnancy. The association between low gynecological age and preterm labor is presumed to reflect an irritability of the adolescent uterus, a sensitivity to dehydration, and/or an altered hormonal milieu that promotes maternal development at the expense of fetal well-being.
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PMID:Young maternal age and preterm labor. 927 49

Hypertonic saline (HS) has been shown to decrease intracranial pressure (ICP) and cerebral water content in experimental models of traumatic brain injury (TBI). The purpose of the present study was to test the efficacy of administration of HS (7.5%) combined with 6% hydroxyethyl starch (molecular weight 200.000/0.60-0.66; HHES) for the treatment of therapy-resistant intracranial hypertension in patients with severe TBI. Six patients with severe TBI (GCS < 8) who met the inclusion criteria (therapy resistant ICP > 25 mmHg, cerebral perfusion pressure (CPP) < 60 mmHg, plasma-Na+ < 150 mOsm and > 4 hours since the last HS/HHES treatment) were prospectively enrolled in the study and received between one and ten bolus infusions of maximal 250 ml HS/HHES at a rate of 20 ml/min. A total of 32 infusions were given. Administration of HS/HHES significantly lowered ICP by 44% and improved CPP by 38% to well above 70 mmHg at 30 min without affecting arterial blood pressure or blood gases. Plasma sodium normalized within 30 min. Experimental studies from our laboratory indicate that the ICP lowering effect is primarily due to dehydration of brain tissue and that cerebral blood volume remains largely unaffected by HS. In summary, HS/HHES reduces otherwise therapy-resistant intracranial hypertension and improves cerebral perfusion even after repeated administration without negatively affecting blood pressure or causing a rebound ICP increase.
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PMID:Hypertonic/hyperoncotic saline reliably reduces ICP in severely head-injured patients with intracranial hypertension. 941 99

The most common diagnoses of elderly patients in the emergency department (ED) were compared among three age subgroups: 65 to 74, 75 to 84, and 85 and older. The computerized billing records for patient visits to 10 northern New Jersey hospital EDs for the years 1985 to 1991 were retrospectively analyzed. The most frequently occurring ICD-9-CM codes for elderly patients were compared among the three age subgroups. Elderly persons comprised 174, 146 (14% of the total) patient visits. The 176,146 patient visits were assigned 259,440 ICD-9-CM codes. The most common ICD-9-CM codes for medical diagnoses included chest pain, cardiac dysrhythmias, congestive heart failure, syncope, abdominal pain, and dyspnea. Fractures, particularly of the lower limb and upper limb; contusions; open wounds, particularly of the head, neck, and trunk; and falls were among the most common trauma diagnoses. The proportions in the three age subgroups of each diagnosis were statistically significantly different, except for cardiac arrest and contusions of the trunk and of multiple sites. The diagnoses with clinically significant higher relative risks in older age subgroups were atrial fibrillation, congestive heart failure, syncope, hypovolemia/dehydration, gastrointestinal hemorrhage, dyspnea, pneumonia, pulmonary edema, cerebrovascular accident, septicemia, urinary tract infection, fractures, and open wounds of the head, neck, trunk, particularly the scalp, and falls. Clinically significant lower relative risks were found in older age subgroups for chest pain, acute myocardial infarction, hypertension, angina, chronic airway obstruction not elsewhere classified, epistaxis, contusions of the upper limb, and open wounds of the finger.
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PMID:Age-related differences in diagnoses within the elderly population. 945 12

Taurine is a sulfonic beta-amino acid which occurs in the highest concentration in the brain, the retina and in the myocardium. In cardiomyocytes it presents about 50% of free amino acids and plays a role as an osmoregulator, an inotropic factor and has an antiarrhythmic property. Moreover, taurine lowers arterial pressure by extension of diuresis and by vasodilatation. Similar effect on the vascular system and arterial pressure is exerted by atrial natriuretic peptide (ANP). Increase of both ANP secretion and myocardial taurine concentration is present in the same diseases as congestive cardiac failure, hypertension and hypernatremia. The aim of the study was the evaluation of general taurine depletion, caused by making the rats drink guanidinoethyl sulfonate (GES)--an inhibitor of taurine transport affecting fluid balance and arterial pressure as well as plasma ANP concentration under normal conditions and after increase of sodium load. The 103 male Wistar rats weighing 250-300 g were used. The animals were separated into 5 groups. Control group received tap water to drink. Group II was sodium-loaded by drinking 171 mmol/l NaCl. In group III depletion of taurine was obtained by the intake of 60 mmol/l GES. Rats in group IV were drinking 60 mmol/l GES in 171 mmol/l NaCl. Group V was made to drink 200 mmol/l taurine in 171 mmol/l NaCl. All animals had standard food and were able at any time to drink. Duration of the experiment was 20 days. At the onset and after 10 and 20 days the rats were weighed and their systolic blood pressure was measured by tail plethysmography. After 10 and 20 days of the study, plasma and myocardium taurine concentration, ANP, hematocrit, plasma osmolity, natremia, kalemia, urea and creatinine concentrations were determined. Taking GES for 20 days led to 43% decrease of plasma taurine and its myocardium content about 50% as compared to control group (Tab. 2). High, statistically significant correlation (r = 0.50, p < 0.001) between myocardium taurine and plasma ANP was found. The animals with taurine depletion had significantly lower (about 30%) plasma ANP concentration (Tab. 3), higher natremia (Tab. 4) and their arterial pressure increased due to sodium load. Systolic pressure was 11 mm Hg higher in that group in comparison to control and other groups (Tab. 1). However, the sodium-loading of the rats that drank taurine solution led to an increase of hematocrit, plasma osmolity, urea concentration and body mass gain as compared to control group, but without any arterial pressure increase. The sodium-loaded rats with normal plasma and myocardium taurine concentration were affected in a similar manner. The rats with higher myocardium taurine concentration had lower heart mass index. Results of this work lead to the following conclusions: 1. Depletion of taurine in hearts of examined rats leads to a decrease of plasma atrial natriuretic peptide (ANP) concentration in plasma. 2. ANP secretion caused by salt loading is lower in animals with taurine depletion than in normal animals. 3. Sodium-loading of animals with taurine depletion leads to hypernatremia and to an increase of arterial pressure. 4. Addition of taurine to animals loaded with sodium may lead to their dehydration.
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PMID:[Taurine as a regulator of fluid-electrolyte balance and arterial pressure]. 947 12

The purpose of the present study was to analyze the long-term regulation of renal bumetanide-sensitive Na+-K+-2Cl- cotransporter and thiazide-sensitive Na+-Cl- cotransporter gene expression during changes in NaCl and water metabolism. Male Wistar rats exposed to high or low NaCl intake, saline loading, dehydration, water loading, and furosemide administration during 7 days were studied. Control groups had access to regular food and tap water. Rats were kept in metabolic cages for 4 days before and during the experiment to determine daily urinary electrolyte excretion and osmolarity. At the end of the experiment, creatinine clearance and serum electrolyte levels were also measured. Kidneys were excised and macroscopically subdivided into cortex and outer and inner medulla. Total RNA was extracted from each individual cortex or outer medulla by use of the guanidine/cesium chloride method. The Na+-K+-2Cl- cotransporter expression in outer medulla total RNA was assessed by nonradioactive Northern blot analysis and the Na+-Cl- cotransporter expression in renal cortex total RNA was assessed by semiquantitative polymerase chain reaction. Experimental maneuvers were adequately tolerated, and all groups developed the appropriate renal response to each challenge. However, the level of expression of both cotransporters did not change in any model, except for a 2.8-fold increase in the Na+-Cl- cotransporter expression during dehydration. We conclude that nephron adaptation to 7-day modifications in NaCl and water metabolism does not include changes in the amount of electroneutral sodium-coupled cotransporter gene expression at the mRNA level.
Hypertension 1998 Apr
PMID:Electroneutral Na-coupled cotransporter expression in the kidney during variations of NaCl and water metabolism. 953 27

Renal vein thrombosis (RVT) is the most frequently occurring vascular condition in the new-born kidney. The predisposing factors include dehydration, sepsis, birth asphyxia, maternal diabetes, polycythaemia and the presence of an indwelling umbilical venous catheter. (RVT) may present clinically with a flank mass, haematuria, hypertension or renal failure. Many imaging modalities have been employed, but ultrasound is the technique most commonly used in the evaluation of neonates with suspected RVT. Thrombosis commences in the small renal veins and subsequently propagates via larger interlobar veins to the main renal vein and inferior vena cava (IVC). The ultrasound appearances depend upon the stage at which the examination is performed and extent of the thrombus. Initially, the interlobular and interlobar thrombus appears as highly echogenic streaks. These streaks commence in a peripheral, focal segment of the involved kidney and only persist for a few days. In the first week the affected kidney swells and becomes echogenic with prominent echopoor medullary pyramids. Later, the swelling increases and the kidney becomes heterogenous with loss of corticomedullary differentiation. Grey scale ultrasound readily demonstrates thrombus within the renal vein and IVC. Adrenal haemorrhage is a recognized association and may be identified ultrasonically. Colour Doppler scanning provides additional information. In the early stages of RVT, colour Doppler may demonstrate absent intrarenal and renal venous flow. Ultimately, the kidney may recover, show focal scarring or become atrophic. Thus, ultrasound provides an accessible and reliable tool in the assessment of suspected neonatal RVT.
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PMID:The ultrasound appearances of neonatal renal vein thrombosis. 953 15

Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension and heart failure. However, acute renal failure (ARF) may occur in patients who are taking these drugs in situations associated with decreased glomerular filtration pressure, such as dehydration caused by acute diarrhea or diuretic therapy. Sixty-four patients who were admitted to the intensive care unit for ARF associated with ACE inhibitor therapy were followed for more than 5 years. In this historical retrospective study, we documented that 45 patients were treated for hypertension (group I) and 19 were treated for heart failure (group II). Their mean age was 71.2+/-11.6 years. Patients with ARF presented with overt dehydration in 91% and 84% of the cases in groups I and II, respectively. Hypovolemia was caused by diuretics or gastrointestinal fluid loss. Bilateral artery-renal stenosis or stenosis in a solitary kidney was documented in 22% and 10% of patients in groups I and II, respectively. The probability of survival was 91% and 49% at 1 year and 64% and 18% at 5 years, for groups I and II, respectively. Acute renal failure required hemodialysis in seven patients, but none of them became dialysis dependent. In the subgroup of patients with preexisting chronic renal failure, all the patients except for one who belonged to group II died within 2 years. In both groups, after resolution of ARF, plasma creatinine concentration returned to baseline level and the course of renal function was not significantly worsened. In conclusion, ARF associated with ACE inhibitors is likely to occur in many patients without renal artery stenosis after unexpected dehydration, especially in older patients with congestive heart failure. In both groups of patients, in the absence of preexisting chronic uremia, recovery of renal function occurred without sequelae, even after an episode of acute tubular necrosis requiring dialysis.
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PMID:Long-term follow-up of acute renal failure caused by angiotensin converting enzyme inhibitors. 1056 Jul 94

A comprehensive review of the literature through mid-1997 is presented on the application of immediate early gene mapping to problems related to brain mechanisms of fluid homeostasis and cardiovascular regulation in mammals. First, the basic mechanisms of fluid intake and the principles and pitfalls of immediate early gene mapping are briefly introduced. Then, data from several principal paradigms are reviewed. These include fluid deprivation and intracellular dehydration, both of which are associated with thirst and water intake. The contributions of peripheral sodium receptors, and of both hindbrain and forebrain integrative mechanisms are evaluated. Extracellular dehydration, and associated aspects of both thirst and sodium appetite are then reviewed. The contributions of both structures along the lamina terminalis and the hypothalamic magnocellular neurosecretory groups figure prominently in most of these paradigms. Effects of hypotension and hypertension are discussed, including data from the endogenous generation and the exogenous application of angiotensin II. Lastly, we summarize the contribution of the early gene mapping technique and consider briefly the prospects for new advances using this method.
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PMID:Brain mechanisms of mammalian fluid homeostasis: insights from use of immediate early gene mapping. 986 12

Angiotensin (Ang) type 1a (AT1a) receptors are critical in the control of blood pressure and water balance. Experiments were performed to determine the influence of dehydration on brain Ang receptors and plasma vasopressin (VP) in mice lacking this receptor. Control or AT1a knockout (AT1aKO) male mice were give water ad libitum or deprived of water for 48 hours. Animals were anesthetized with halothane, blood samples were collected by heart puncture, and brains were processed for Ang-receptor autoradiography with 125I-sarthran (0.4 nmol/L). Dehydration produced an increase in AT1 receptors in the paraventricular nucleus (PVN) and anterior pituitary (AP) in control mice (PVN: 70+/-16 versus 146+/-10 fmol/mg protein; AP: 41+/-7 versus 86+/-15 fmol/mg protein). No changes were noted in the median preoptic nucleus. The majority of the brain receptors were of the AT1 subtype. There was little or no specific Ang binding in AT1aKO mice and no effect of dehydration. Plasma VP levels were elevated in the halothane-anesthetized animals (>200 pg/mL) with no significant effect of dehydration. A separate experiment was performed with decapitated mice anesthetized with pentobarbital. Dehydration increased plasma VP in control mice, from 3.3+/-0.6 to 13.3+/-4.7 pg/mL, whereas no change was noted in the AT1aKO mice, 5.1+/-0.3 versus 6.1+/-0.7 pg/mL (water versus dehydration). These results demonstrate a differential response to dehydration in mice lacking AT1a receptors. There was no evidence for AT1 receptors of any subtype in the brain regions examined and no effect of dehydration on VP secretion or brain Ang receptors.
Hypertension 1999 Jan
PMID:Neuroendocrine effects of dehydration in mice lacking the angiotensin AT1a receptor. 993 Nov 52

Nephropathy may develop in patients with type 1 diabetes because poor glycemic control produces effects that eventually lead to glomerular scarring and renal failure. The worse and more prolonged the hyperglycemia, the greater the risk of diabetic nephropathy. In patients with type 2 diabetes, hyperglycemia, as well as insulin resistance and generalized vascular disease, is involved in the pathogenesis of nephropathy. The glomerular changes of early diabetic nephropathy can be identified only by renal biopsy or by testing for microalbuminuria. Once macroalbuminuria occurs (albumin excretion rate, > 300 mg/day), usually after type 1 diabetes has been present for 10 to 15 postpubertal years, end-stage renal disease is almost inevitable. However, aggressive control of hypertension in diabetic patients without microalbuminuria helps avoid nephropathy, and tight glycemic control in those with microalbuminuria can avoid or delay its onset. Even when macroalbuminuria is present, treatment can prolong renal function. Aggressive antihypertensive therapy, especially with ACE inhibitors, can reduce renal decline by half. Avoiding circumstances that may damage the kidneys (e.g., use of radiocontrast materials or nephrotoxic drugs, dehydration, hyperlipidemia, urinary tract infection, buildup of AGEs) is critical. Some treatment methods are controversial (dietary protein restriction) or still under investigation (use of injected or oral heparin) but may help delay renal transplantation or dialysis.
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PMID:Dealing with diabetic nephropathy. 1002 5


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