title: Postnatal development of renal sodium handling in premature infants.
abstract: To estimate the contribution of the specific defect in proximal and distal tubular reabsorption of sodium to renal salt wasting, fractional sodium excretion, distal tubular sodium delivery, and distal tubular sodium reabsorption were determined in 11 healthy premature infants. The study was performed on the seventh day and at weekly intervals thereafter up to the sixth week of life. Sodium clearance and fractional sodium excretion decreased significantly with increasing postnatal age (P less than 0.001). There was no significant alteration in either osmolar or free-water clearances. Distal tubular sodium delivery steadily decreased from 4.96 +/- 0.66 (mean +/- SE) in the first week to 3.3 +/- 0.41 ml/minute/dl GFR in the sixth week of life (P less than 0.05). Distal tubular sodium reabsorption was 69.5 +/- 2.36% in the first week, then rose significantly to reach a value of 83.7 +/- 1.85% in the second week (P less than 0.001) and remained practically unchanged thereafter. It is suggested that the rapid improvement of distal tubular sodium reabsorption in premature infants might result from forced stimulation by the excessively activated renin-angiotensin-aldosterone system.
mesh_terms: D000367:Age Factors; D000450:Aldosterone / Q000378:metabolism; D000804:Angiotensin II / Q000378:metabolism; D004231:Diuresis; D005919:Glomerular Filtration Rate; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007234:Infant, Premature; D007684:Kidney Tubules / Q000378:metabolism*; D008137:Longitudinal Studies; D008297:Male; D009318:Natriuresis; D009994:Osmolar Concentration; D012083:Renin / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*
chemical_list: D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D012083:Renin