ABSTRACT:In the neonatal period, the human kidney is characterized by an impaired ability to regulate water and sodium homeostasis, resembling partial aldosterone resistance. The aim of our study was to assess this hormonal insensitivity in newborn infants and to determine its relationship with neonatal sodium handling. We conducted a prospective study in 48 healthy newborns and their mothers. Aldosterone, renin, and electrolyte concentrations were measured in umbilical cords and in maternal plasma. Urinary aldosterone concentrations and sodium excretion were determined at urination within 24 h after birth. A significant difference was observed between aldosterone and renin levels in newborn infants compared with their mothers (817 Ϯ 73 versus 575 Ϯ 55 pg/mL and 79 Ϯ 10 versus 15 Ϯ 2 pg/mL, respectively, p Ͻ 0.001). This hyperactivation of the renin-angiotensin-aldosterone system was associated with hyponatremia and hyperkalemia in the newborn infants, and high urinary sodium loss, consistent with a partial aldosterone resistance at birth. Unlike plasma aldosterone, urinary aldosterone concentration was found highly correlated with plasma potassium concentrations, thus representing the best index for accurate evaluation of mineralocorticoid sensitivity. Our study represents a comprehensive characterization of the renin-aldosterone axis in newborn infants and provides evidence for physiologic partial aldosterone resistance in the neonatal period. (Pediatr Res 66: 323-328, 2009) T he human kidney displays a tubular immaturity at birth, with sodium waste, responsible for a negative sodium balance, and an impaired ability to reabsorb water (1), which is aggravated under circumstances such as prematurity, pyelonephritis, and gastroenteritis (2). This inability to maintain homeostatic functions is a major problem encountered by pediatricians, most notably in preterm infants. Indeed, the challenge is to find a balance between the lethal risk of dehydration and the associated morbidity of excessive hydromineral supplementation, contributing to severe complications such as intraventricular hemorrhage and bronchopulmonary dysplasia (3). A better understanding of water and sodium regulation in the neonatal period is a prerequisite to propose new therapeutic strategies for the management of preterm infants.Sodium reabsorption is mainly controlled by aldosterone, a steroid hormone synthesized in the zona glomerulosa of the adrenal gland, secondary to renin stimulation via angiotensin II and to potassium stimulation (4). In the distal nephron, aldosterone, by binding to its receptor, the mineralocorticoid receptor, a transcription factor (5), tightly regulates the expression and the activity of several transport proteins implicated in sodium, potassium, and water homeostasis, as the alpha subunit of the epithelial sodium channel (6), the Na-KATPase (7), and the aquaporin 2 (8). A possible role of a partial and transient tubular unresponsiveness to this hormone has been suggested to account for sodium waste in neonates (9,10)....

Liver antioxidant enzyme activities were high in patients with NAFLD, reflecting an oxidative stress possibly involved in inflammation and fibrogenesis. However, erythrocyte and plasma antioxidant defenses did not reflect intrahepatic peroxidation.

Respiratory-related variabilities in stroke volume and arterial pulse pressure (Delta%Pp) are proposed to predict fluid responsiveness. We investigated the influence of tidal volume (Vt) and adrenergic tone on these variables in mechanically ventilated patients. Cyclic changes in aortic velocity-time integrals (Delta%VTI(Ao), echocardiography) and Delta%Pp (catheter) were measured simultaneously before and after intravascular volume expansion, and Vt was randomly varied below and above its basal value. Intravascular volume expansion was performed by hydroxyethyl starch (100 mL, 60 s). Receiver operating characteristic curves were generated for Delta%VTI(Ao), Delta%Pp and left ventricle cross-sectional end-diastolic area (echocardiography), considering the change in stroke volume after intravascular volume expansion (> or =15%) as the response criterion. Covariance analysis was used to test the influence of Vt on Delta%VTI(Ao) and Delta%Pp. Twenty-one patients were prospectively included; 9 patients (43%) were responders to intravascular volume expansion. Delta%VTI(Ao) and Delta%Pp were higher in responders compared with nonresponders. Predictive values of Delta%VTI(Ao) and Delta%Pp were similar (threshold: 20.4% and 10.0%, respectively) and higher than that of left ventricle cross-sectional end-diastolic area at the appropriate level of Vt. Delta%Pp was slightly correlated with norepinephrine dosage. Delta%Pp increased with the increase in the level of Vt both before and after intravascular volume expansion, contrasting with an unexpected stability of Delta%VTI(Ao). In conclusion, Delta%VTI(Ao) and Delta%Pp are good predictors of intravascular fluid responsiveness but the divergent evolution of these two variables when Vt was increased needs further explanation.