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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a prospective study we estimated common renal parameters in 48 full term normal neonates, of which 15 were also tested at 6 months and 12 months of age. The mean levels of serum creatinine, were high at birth (0.73 mg/dl) but normal for age at 6 and 12 months; uric acid followed a similar trend. The blood pH and bicarbonate were low at birth (7.28 and 20.36 mEq/L, respectively) reached normal adult values by 12 months; chloride levels were high at birth (110 +/- 5 mEq/L) and normal at 6 months. The plasma renin activity was higher than normal all throughout the first year (27.1, 416.8, 64.8 ng/ml/hr by RIA). Plasma aldosterone values were high at birth (1387.5 pg/ml) and reached normal level (301.6) at 12 months. Renal length and volume as assessed by ultrasonography compared well with American standards. Urinary constituents were variable due to breast feeding up to 6 months and varied diet during the weaning period. This study shows that mild metabolic acidosis and hyperchloremia due to immaturity of renal acidification mechanism and high renin and aldosterone levels due to partial nonresponsiveness of distal tubules are normal variables in babies from birth to 6 months. The levels of serum creatinine and uric acid are high at birth and in assessing renal functions this should be borne in mind.
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PMID:Renal parameters during infancy. 129 93

The circulating levels of vasopressin, catecholamines and renin activity before, during and following a 10-20% fall in mean arterial blood pressure induced by sodium nitroprusside were measured in six chronically catheterized lambs during the first week of life. No significant changes in pHa, PaO2, PaCO2, Plasma sodium or osmolality were observed during or following the infusion of sodium nitroprusside at an average of 12 g.kg-1.min-1 (table I). However, the fall in blood pressure at the end of 60 minutes infusion, was associated with significant increases in the plasma levels of vasopressin from a control value of 2.4 +/- 0.57 to a maximum of 35.1 +/- 16.3 pg/ml (p = .002), renin activity from 6.7 +/- 1.56 to 27.4 +/- 11.44 ng.ml-1.hr-1 (p = .003), and catecholamines from 189.3 +/- 42.15 to 543.3 +/- 100.52 pg.ml-1 (p = .0001). The increase in vasopressin is lower, while that of PRA was higher and catecholamines similar to those found in the ewe. Plasma renin activity (PRA) and catecholamine levels remained elevated for at least 30 minutes following the end of the infusion while the mean blood pressure rose significantly above control levels and remained elevated for twenty minutes. We speculate that the persistent elevated levels of vasoactive mediators are responsible for the prolonged rebound hypertension following the cessation of the nitroprusside infusion and is the result of an immaturity of either a feedback process or metabolism of the vasoactive mediators or a combination of both mechanisms. This rebound hypertension could have adverse effects particularly in the very immature neonate.
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PMID:Plasma vasopressin, renin and catecholamines during nitroprusside-induced hypotension in the newborn lamb. 269 75

Shortly after birth, a 1,860-g premature male newborn with respiratory distress syndrome had brisk diuresis, rapid weight loss, and severe hyponatremia despite aggressive Na+ and fluid replacement. The serum cortisol level was normal, and the 17-OH progesterone concentration was low. He did not show any response to treatment with dexamethasone and desoxycorticosterone acetate. Results of renal function studies were within the normal range for his gestational age. The serum aldosterone level and plasma renin activity were grossly elevated, confirming the diagnosis of pseudohypoaldosteronism. This uniquely early and dramatic presentation was attributed to immaturity of the proximal renal tubule at 32 weeks' gestation. The subsequent improvement paralleled the rapid maturation of the kidney after birth.
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PMID:Pseudohypoaldosteronism. 634 58

Plasma renin (PRC) and aldosterone concentrations are known to be high during early postnatal life. Whether this is related to the low rates of renal blood flow or to sodium homeostasis remains unknown. Measurement of PRC, renal blood flow, and its intrarenal distribution were performed in 1- to 3-wk-old puppies subjected to maneuvers known to stimulate or inhibit renin release. In the awake state, PRC was observed to be higher in 2-wk-old puppies than in older or younger dogs, (P less than 0.0001). Significant differences in PRC were also found between litters (P less than 0.0001), but they did not account for the age-related changes. Anesthesia resulted in a 3- to 5-fold rise in PRC, whereas saline expansion suppressed PRC at all ages, the fall tending to become progressively greater with age (P less than 0.09). There was no significant correlation between the age-related changes in PRC and those in renal blood flow or its intrarenal distribution. The results of these experiments demonstrate that in the newborn from a qualitative point of view, PRC changes appropriately in response to various stimuli. However, quantitative age-related differences exist in this regard, reflecting an initial immaturity of the feedback system.
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PMID:The renin angiotensin system in newborn dogs: developmental patterns and response to acute saline loading. 699 Mar 67

The concentrations of aldosterone in the plasma and adrenal glands, the concentrations of sodium and potassium in the plasma and the hematocrit were estimated from birth to day 6 after birth in premature mice removed by Caesarean section on day 19 of pregnancy in comparison with newborn mice delivered spontaneously vaginally on day 20 of pregnancy. In premature mice, the plasma aldosterone concentrations increased twice: at birth after reanimation, then at 6 h after birth. The first increase at birth resulted probably from ACTH stimulation. Several factors could be involved in the peak at 6 h after birth: ACTH stimulation, the decrease in the level of sodium in the plasma and the increase in the hematocrit due to kidney immaturity of premature mice. The results suggest that the renin-angiotensin-aldosterone system is able to respond to stimulations in the first 6 h after birth in premature mice. The rise in the level of plasma aldosterone which has been found at birth in newborns delivered spontaneously vaginally on day 20 of pregnancy (control animals) did not result from variations of plasma electrolytes, plasma volume and ACTH; this rise has been induced by labor of the parturition which caused the aldosterone release from adrenal glands.
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PMID:Plasma and adrenal aldosterone levels in premature mice at birth and during neonatal development. 718 5

Plasma aldosterone (A), corticosterone (B), deoxycorticosterone (DOC), progesterone (P), 17-hydroxyprogesterone (17-OHP), cortisol (F), and cortisone (E) were measured simultaneously by specific radioimmunoassays in small plasma samples obtained from 174 normal infants and children between 2 hr and 15 yr of age. The significantly elevated neonatal mean levels (ng/ml) of 2.5 (A), 4.1 (DOC), 53.0 (P), and 6.6 (17-OHP) dropped significantly during infancy reaching prepubertal levels between 3 months and 3 yr of age, with a transient, significant DOC increase between 1--7 yr. The glucocorticoids F andB declined significantly from means of 68 and 4.4 to 11.4 and 0.28 ng/ml, respectively, during the first weeks of life, then increased significantly reaching adult levels between 1--3 yr of age. Mean E fell progressively from 74 ng/ml after birth to 10 ng/ml during 1--5 yr (P less than 0.0001), then slightly increased to adult levels. After age 7 yr, P and 17-OHP, in contrast to the other steroids, rose significantly in both boys and girls relative to pubertal development. The observed changes are thought to be due to (1) adaptation of the adrenal neocortex to extrauterine life after disruption of the fetoplacental unit, (2) a physiologic lack of corticosteroid binding globulin (CBG) during infancy due to maturation of hepatic CBG biosynthesis, (3) the functional immaturity of the infant kidney compensated by an increased activity of the renin-angiotensin-aldosterone system, and (4) gradually increasing gonadal secretion of progestins during puberty.
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PMID:Plasma levels of aldosterone, corticosterone, 11-deoxycorticosterone, progesterone, 17-hydroxyprogesterone, cortisol, and cortisone during infancy and childhood. 736 May 20

In postnatal animals, carotid occlusion does not stimulate reflex hormonal responses, because decreases in carotid arterial baroreceptor activity are balanced by reflex-mediated increases in vagal afferent traffic from aortic and cardiac receptors. The present experiments were designed to test the hypothesis that hormonal responses to carotid occlusion in fetal animals are not inhibited by vagal afferents. In thirteen chronically catheterized fetal sheep (125-146 days), bilateral carotid occlusion (n = 11) increased arterial blood pressure from 44.0 +/- 2.4 to 55.2 +/- 3.3 mmHg, decreased heart rate from 189 +/- 5 to 165 +/- 12 beats/min, increased plasma adrenocorticotropin from 71 +/- 15 to 248 +/- 79 pg/ml and vasopressin from 3.0 +/- 1.0 to 7.4 +/- 2.6 pg/ml but did not significantly alter renin. Plasma hormone concentrations were not significantly altered in control (n = 7) experiments or in response to unilateral carotid occlusion (n = 4). The results of these experiments demonstrate the functional immaturity of the vagal afferent buffering systems in the late-gestation fetus compared with the postnatal animal.
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PMID:Fetal responses to carotid occlusion: immaturity of buffering systems. 786 27

The mature, fully differentiated connecting tubule (CNT) cell plays an important role in the regulation of serum potassium levels and synthesizes the enzyme tissue kallikrein, a main component of a renal vasoactive system, the kallikrein-kinin system. To characterize the growth of CNT cells (tissue kallikrein-producing cells), we studied the rat kidney at three different time points of postnatal development: at day 5, day 15, and day 30. The CNT cells were identified on tissue sections by a standardized immunohistochemical procedure. The tissue kallikrein content was determined by radioimmunoassay and the activity of the enzyme in kidney homogenates was measured using a selective synthetic substrate. The number of immunolabeled CNT and CNT cells per cortex area gradually increased from day 5 to day 30. A similar rise in the content and activity of tissue kallikrein was observed when the enzyme levels were determined by radioimmunoassay or by the enzymatic method. In addition, the morphometric analysis showed that the distal end of CNT had larger cells that displayed a more intense tissue kallikrein staining than those present in the proximal end, suggesting that the postnatal development of CNT is induced from its juxtamedullary portion. Our results show that tissue kallikrein expression is very low in the newborn rat, increasing gradually with age to reach adult levels at day 30. This finding, together with the morphometric data, suggests immaturity of CNT cells in newborn rats, a fact that could contribute to explaining the high serum potassium levels reported at this stage. In addition, the contrasting behavior of kallikrein and renin in the postnatal development (kallikrein increasing and renin decreasing) could explain the gradual decrease in renal vascular resistance and increase in renal blood flow observed after birth.
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PMID:Postnatal maturation of tissue kallikrein-producing cells (connecting tubule cells) in the rat kidney: a morphometric and immunohistochemical study. 854 32

Understanding the mechanisms of fetal obstructive uropathy will be essential for the specific management of the wide clinical spectrum of congenital obstructive conditions, including selecting observational therapy for mild cases and attempting to maximize renal function in severe cases. Recognition of the unique aspects of fetal renal obstruction is essential to formulate a useful research program, as the lessons of postnatal acquired obstruction are not directly transferable to congenital obstruction. Experimental studies of renal obstruction have demonstrated alterations in the developmental regulation of growth and differentiation in the fetal kidney. Depending on the gestational timing and severity of obstruction, growth may be impaired or accelerated. Similarly, patterns of altered differentiation may indicate immaturity or accelerated maturation, as well as aberrant differentiation. Concomitant with altered development, there is evidence that normal renal regulatory mechanisms, including the renin-angiotensin system and renal hemodynamics, may be affected by obstruction, possibly as compensatory responses. The mechanisms of these various alterations remain to be defined, but are likely to involve combinations of biomechanical signal transduction, growth factor expression, and responses of specific renal autoregulatory mechanisms. Fetal renal obstruction remains incompletely defined. The body of experimental evidence indicates that investigation of mechanisms regulating growth and differentiation is likely to yield important understanding of fetal renal obstruction to permit more accurate prognosis and management. Viewing fetal renal obstruction as a disorder of kidney development, with disordered growth and differentiation, suggests a definition of obstruction as a condition, that--if uncorrected--will lead to impairment in the ultimate functional potential of the kidney. Intervention should aim to maximize functional potential rather than to simply maintain the status quo.
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PMID:Obstruction of the fetal urinary tract. 1049 96

Angiotensin-converting enzyme (ACE) has an active role in the control of blood pressure and body fluid homeostasis both before and after birth. This study investigated the ontogeny of pulmonary and renal ACE concentrations in fetal and neonatal horses. Fetal pulmonary ACE concentration increased from 250 days towards term (c. 335 days). Newborn foals showed significantly higher mean concentrations of pulmonary ACE (4.40 +/- 0.62 nmol min(-1) mg protein(-1)) than both fetuses during late gestation (1.23 +/- 0.51 nmol min(-1) mg protein(-1)) and animals aged 1 day to 2 weeks of postnatal age (0.85 +/- 0.15 nmol min(-1) mg protein(-1)). Renal ACE was detected in fetal horses from 100 days of gestation but showed no developmental trend during the second half of gestation or in early postnatal life. Overall in the fetus, mean concentrations of renal ACE were also approximately 10 times lower than mean pulmonary values. Renal ACE concentration may be related to the functional immaturity of the equine kidneys. The increase in pulmonary ACE concentration seen towards term in the fetal horse may be induced by the prepartum cortisol surge that occurs very close to delivery in this species. Therefore, premature delivery in this species may interrupt the onset of ACE production in the fetal lungs and circumvent the normal maturation of the renin-angiotensin system.
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PMID:Developmental changes in pulmonary and renal angiotensin-converting enzyme concentration in fetal and neonatal horses. 1261 84


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