Details

Autor(en) / Beteiligte

• Kalhoff, H
• Manz, F
• Diekmann, L
• Kunz, C
• Stock, GJ
• Weisser, F

Titel

Decreased growth rate of low-birth-weight infants with prolonged maximum renal acid stimulation

Ist Teil von

• Acta Paediatrica, 1993-06, Vol.82 (6-7), p.522-527

Ort / Verlag

Oxford, UK: Blackwell Publishing Ltd

Erscheinungsjahr

1993

Quelle

MEDLINE

Beschreibungen/Notizen

• In a prospective randomized study, the urine pH of 170 premature and small‐for‐gestational‐age (SGA) newborns was routinely screened to detect patients with spontaneously developing maximum renal acid stimulation, an obligatory early stage in the development of late metabolic acidosis. Nitrogen assimilation was evaluated from the ratio of urinary nitrogen excretion and intake. Forty‐two premature infants and 10 SGA prematures and newborns after intensive care therapy with body weights greater than 1.5 kg and 25 prematures (including 7 SGA infants) with body weights less than 1.5 kg, spontaneously showed urine pH values below 5.4 on two consecutive days, suggesting maximum renal acid stimulation. These patients were randomly given either oral alkali therapy with sodium bicarbonate 2 mmol/kg/day or no therapy for a period of seven days. In both groups, urine pH was controlled daily. Patients in the control group without alkali therapy and with urine pH values less than 5.4 for seven days showed a significant decrease in weight gain and a tendency to decreased nitrogen assimilation. We assume that a regular check of urine pH in low‐birth‐weight infants is a useful non‐invasive method of detecting patients in the early stages of development of late metabolic acidosis, i.e. in the stage of “incipient late metabolic acidosis”. This would procide the possibility of starting early effective therapy and thereby reduce the mean duration of admission to neonatal wards. Regarding the risk of a high renal acid load causing the development of late metabolic acidosis in very low‐birth‐weight infants, standard formulas for premature infants should be re‐evaluated with the aim of reducing renal acid load leaving a larger renal surplus capacity for renal acid excretion.