EVALUATION OF ANTIBIOTIC-INDUCED NEPHROTOXICITY IN PRETERM NEONATES BY DETERMINING URINARY ALPHA(1)-MICROGLOBULIN

alpha(1)-Microglobulin (alpha(1)-m, protein HC), a relatively low mole cular weight protein of about 31,000 daltons, was measured in urine of three groups of 34 preterm neonates: group A consisted of 9 healthy p reterm neonates; groups B (n = 13) and C (n = 12) consisted of preterm neonates with suspected or confirmed bacterial infections. Immediatel y after birth, all group B neonates were treated with ampicillin and a ztreonam in combination, and all group C neonates were treated with ox acillin and amikacin in combination. To optimize amikacin administrati on, computerized individually tailored doses were administered. Urine samples were obtained from a short collection in sterile bags on the I st, 4th, and 7th day after delivery in all infants. Urinary alpha(1)-m concentrations were measured by a turbidimetric method (latex aggluti nation photometric immunoassay) and results were expressed as a ratio to urinary creatinine. In group A, urinary alpha(1)-m concentrations w ere stable after birth. In group C, alpha(1)-m excretion increased imm ediately within the 1st day of treatment, and over the 1st week of lif e urinary alpha(1)-m levels were significantly higher than in group A (P = 0.033). These data support the conclusion that amikacin administr ation was the most important factor inducing renal tubular dysfunction in the neonates of group C.