Manz F, Diekmann L, Kalhoff H, von Kries R, Raupp P, Stock G J, Tölle H G
Forschungsinstitut für Kinderernährung, Dortmund, FRG.
Child Nephrol Urol. 1991;11(4):193-5.
In 40 premature infants fed human milk with an actual gestational age of 261 +/- 16 days and an actual body weight of 1.06-2.75 kg, 44 urine samples were collected, and blood acid-base status was measured on day 32 (+/- 16) of life. In the urine, the following results (mean +/- SD) were obtained: urine pH 6.05 +/- 0.65, titratable acidity 0.24 +/- 0.14 mmol/kg/day, ammonium 0.78 +/- 0.25 mmol/kg/day, net acid excretion 0.83 +/- 0.47 mmol/kg/day. There was no significant correlation between renal net acid or ammonium excretion and actual body weight. However, urine pH was positively correlated with body weight. Obviously, premature infants with an actual body weight below 1.5 kg need a higher stimulation of renal hydrogen ion secretion to excrete the same amount of ammonium than those with an actual body weight of about 2.5 kg. The limited renal acidification capacity of very low birth weight infants is a risk factor for the development of late metabolic acidosis.
在40例实际胎龄为261±16天、实际体重为1.06 - 2.75千克的母乳喂养早产儿中，收集了44份尿液样本，并在出生后第32（±16）天测量了血液酸碱状态。在尿液中，获得了以下结果（平均值±标准差）：尿液pH值6.05±0.65，可滴定酸度0.24±0.14毫摩尔/千克/天，铵0.78±0.25毫摩尔/千克/天，净酸排泄0.83±0.47毫摩尔/千克/天。肾脏净酸排泄或铵排泄与实际体重之间无显著相关性。然而，尿液pH值与体重呈正相关。显然，实际体重低于1.5千克的早产儿比实际体重约2.5千克的早产儿需要更高的肾脏氢离子分泌刺激来排泄相同量的铵。极低出生体重儿有限的肾脏酸化能力是晚期代谢性酸中毒发生的一个危险因素。
