B. Wu et al., HYPERMAGNESIURIA AND HYPERCALCIURIA IN CHILDHOOD LEUKEMIA - AN EFFECTOF AMIKACIN THERAPY, Journal of pediatric hematology/oncology, 18(1), 1996, pp. 86-89
Purpose: The purpose of this study is to assess the effects of amikaci
n on renal proximal tubular function, and on magnesium (Mg) and calciu
m (Ca) status in children treated for acute lymphoblastic leukemia (AL
L). Patients and Methods: Eighteen children (11 male/7 female, ages 2-
18 years) receiving antileukemic therapy (Dana Farber Cancer Institute
protocols 87-001 or 91-001) and admitted for febrile neutropenia to T
he Children's Hospital at Chedoke-McMaster, Hamilton, Ontario were rec
ruited into this descriptive prospective study. Each child was treated
with amikacin (7.5 mg/kg/12 h x 10-14 days) for one or more courses.
Results: No patient demonstrated elevations in amikacin trough levels.
beta(2)-Microglobulinuria, glucosuria, proteinuria, and hyperphosphat
uria were absent. Children (50%) presenting with hypomagnesemia (<0.77
mmol/L) had a significant rise in mean urinary Mg:creatinine (0.46 +/
- 0.27 versus 0.82 +/- 0.38 mmol, mean +/- SD, p < 0.05) in response t
o amikacin therapy and the mean Ca:creatinine ratio increased by 95% a
fter 10-14 days of amikacin treatment. Serum Mg and Ca did not change
notably after treatment, irrespective of initial Mg status. Conclusion
s: Aminoglycoside therapy in children with ALL is not associated with
overt nephrotoxicity. A transient renal leak of Mg and Ca does occur.
Screening of ALL children for mild hypomagnesemia may help to identify
those most at risk of disruption of renal conservation of Mg and poss
ibly Ca.