The effect of intrauterine growth retardation on renal function in the first two months of life.

BACKGROUND: Children born with growth retardation (GR) have a smaller nephron number and are at increased risk for the development of renal disease and hypertension in adult life. Data on the immediate post-natal development of renal function in neonates born with GR are limited and data on the effects of aminoglycosides (AGs) on renal function in these infants are lacking. METHODS: This was a prospective study of 81 preterm neonates with a mean gestational age of 32.5 weeks, 40 born with GR (small for gestational age, SGA) and 41 without GR (appropriate for gestational age, AGA). The infants were classified into 4 groups. Groups A (n = 21) and B (n = 20) consisted of AGA and SGA neonates, respectively, who received AGs, and groups C (n = 20) and D (n = 20) of AGA and SGA neonates, respectively, who did not receive AG treatment. Indices of renal function were: serum creatinine (SeCr), the fractional excretion of sodium (FENa), potassium (FEK), phosphorus (FEP), magnesium and uric acid (FEUA), the urinary calcium/creatinine ratio and the transtubular potassium gradient (TTKG). RESULTS: No differences were observed in the parameters examined between SGA and AGA neonates who did not receive AGs. Conversely, SGA infants who received AGs after birth (group B) exhibited higher values of SeCr 2 months later. Specifically, their mean +/- SD value of SeCr (micromol/l) was 42 +/- 05 compared with 33 +/- 08 in group D, 35 +/- 04 in group A and 33 +/- 04 in group C (P < 0.01). These infants also had significantly higher values of TTKG than SGA infants without AG treatment (22 +/- 9 vs 13 +/- 3 in group D) and FEUA (60 +/- 23 vs 35 +/- 14 in group D). Their FENa and FEP were also inappropriately high despite having lower serum levels of Na and P. CONCLUSION: Preterm SGA infants who had no need of AG treatment after birth have similar renal functional maturation than AGA preterm infants at 2 months of life, but preterm SGA infants who received AGs had indications of impaired glomerular and tubular function at this age.

Genetic risk factors associated with thrombosis in children with congenital neurologic disorders.

Thromboembolic events during the perinatal period are responsible for irreversible brain damage owing to cerebral hypoxia and neuronal necrosis. We investigated the presence of thrombophilia risk factors in children with congenital neurologic disorders. Nineteen children (9 males and 10 females), aged 1 to 14 years (median 4.5 years), who had presented with symptoms and signs of congenital neurologic disorders were studied. Thirty-five age-matched healthy children recruited from the same geographic area served as controls. Three patients of 19 (15.8%) were carrying the factor V Leiden mutation compared with 2 children among the controls (5.7%). One patient was heterozygous for the prothrombin G20210A variant (5.2%) compared with one child who was heterozygous among the controls. Three patients were homozygous (15.8%) and 11 were heterozygous (57.9%) for the C677T 5,10-methylenetetrahydrofolate reductase gene mutation compared with 4 (11.5%) and 18 (51.4%), respectively, among the controls. Three patients of 19 (15.8%) were carrying more than one mutation. We found 18 mutations in 79% (15/19) of the patients and 25 mutations in 69% (24/35) of the healthy children. Among the individuals carrying the homozygous 677TT 5,10-methylenetetrahydrofolate reductase genotype, we found 7 mutations in 32% (6/19) of the patients and 7 mutations in 20% (7/35) of the healthy children (P > .05). In one patient, lupus anticoagulant and antiphospholipid antibodies of IgG isotype were detected. Reduced activities of protein C, protein S, or antithrombin III were not observed in either the patient or the control group. Although, among our cases, we found some well-known risk factors associated with thrombosis in adults, the pathogenesis of these clinical entities remains obscure.