Urinary excretion of 3-methylhistidine in preterm infants (n = 42; 1,712 ± 408 g, 4–91 days old) was 24.2 ± 6 µmol/mmol creatinine or 2.26 ± 0.56 µmol/kg body weight-day. In adults (n = 6; 66 ± 10 kg, 17–50 years), the corresponding values were 10.5 ± 1.1 µmol/mmol creatinine and 2.21 ± 0.23 µmol/kg body weight-day. For both collectives, the breakdown per kg body weight of 3-methylhistidine-containing protein (i.e. actin and myosin) was similar, at approximately 0.7 g/kg·day (preterm infants 0.84, adults 0.60). Since the preterm infants studied contain ∼21% muscle instead of the 43% found in adults, the 3-methylhistidine excretion in preterm infants probably indicates muscle (and intestinal) protein turnover to be about 3 times higher than in adults, a figure in accord with data on whole-body protein turnover in preterm infants and adults (∼ 15 g/kg·day and ∼ 4 g/kg·day, respectively). Urinary excretion of pseudouridine (ψ), 7-methylguanine (m⁷Gua) and N², N²-dimethyl-guanosine (m²₂G) can be used to estimate the turnover of rRNA, mRNA and tRNA, respectively. The values obtained (in µmol/mmol creatinine) in preterm infants are for ψ: 164 ± 32; for m⁷Gua: 39.1 ± 9; and for m²₂ 10.6 ± 2.1. In adults, the values are for ψ: 25.3 ± 3.1; for m⁷Gua: 4.8 ± 0.89; and for m²₂G: 1.53 ± 0.38. This yields 3–4 times higher turnover rates in preterm infants than in adults for all 3 RNA classes: rRNA, 0.1 versus 0.038; tRNA, 1.87 versus 0.66; mRNA 2.35 versus 0.64 µmol/kg·day. Thus all data indicate that preterm infants have a 3- to 4-fold higher turnover than adults not only of whole-body protein, but also of rRNA, tRNA and mRNA.

Creatine and creatinine intake can cause increased urinary creatinine excretion. To estimate the contribution of diet to creatinine excretion in infants, creatine and creatinine were determined in human milk, pasteurized cow's milk and formulas for preterm and term infants. Soy-based formulas did not contain creatine and creatinine. Average concentrations in human milk (creatine 77 [60-100] mumol/l, creatinine 52 [41-65] mumol/l) were markedly lower than in pasteurized cow's milk which contained 598 (476-640) mumol/l creatine and 105 (79-122) mumol/l creatinine. Creatine and creatinine concentrations differed widely in formulas for both preterm and term infants, from 155-559 and 33-174 mumol/l, respectively. The influence of ingested creatine on creatinine excretion should theoretically be negligible. On the other hand, based on known absorption data, creatinine from the diet should increase creatinine excretion in a 3-month-old infant up to an amount in the range of 5.3-28.4% of the endogenous production. Therefore creatinine ingestion should be taken into account when interpreting creatinine excretion in infants.

Single urine voidings were collected twice a week in the clinical course of 12 low-birth-weight infants (gestational age: 31.8 ± 2.8 weeks; birth weight: 1,383 ± 308 g) and analyzed for 3-methylhistidine and creatinine. The mean 3-methylhistidine/creatinine ratio for 6 healthy, well-fed, growing low-birth-weight infants was 20.2 ± 1.9 µmol/mmol. In the clinical course of single individuals a rise of urinary 3-methylhistidine/creatinine ratio was observed in cases of acute infection and/or low energy supply ( < 100 kcal/kg/day) frequently coupled with insufficient weight gain. Mean 3-methylhistidine/creatinine ratios in infants with hyaline membrane syndrome under artificial respiration were generally higher than in the controls matched for energy supply.

3-Methylhistidine and creatinine concentrations were determined in 45 24-hour urine samples collected in 380 single voidings from 23 preterm infants (gestational age: 30–36 weeks, median: 33 weeks; birth weight: 1,613 ± 219 g; age: 9–83 days postpartum) and from 7 infants small for gestational age (birth weight: 2,061 ± 203 g; age: 2–30 days postpartum). Statistical analysis shows that diurnal variations of the ratio 3-methylhistidine/creatinine are negligible. The variability of this ratio is chiefly caused by differences in excretion on different collection dates and is probably due to differences in the metabolic state. Hence the determination of 3-methylhistidine/creatinine ratio in single voidings is sufficient even in low-birth-weight infants. In our collective the mean 3-methylhistidine/creatinine ratio for healthy, well-growing low-birth-weight infants (n = 21) was 19.6 ± 2.3 µmol/mmol. Infants with stagnating or decreasing weight (n = 5) showed 3-methylhistidine/creatinine ratios clearly above that of the normal group.

Weight (LBW) infants fed Human Milk (HM