Abstract：
BACKGROUND:It was shown in animal models and adults that the epidermal growth factor (EGF) is involved in the pathophysiology of calcineurin inhibitor (CNI) induced renal magnesium loss. In children, however, the exact mechanism remains unclear, which was set as the purpose of the present study. METHODS:Children with nephrotic syndrome and renal transplant children treated with CNI (n = 50) and non-CNI treated children (n = 46) were included in this study. Urine and serum samples were collected at three time points to determine magnesium, creatinine, and EGF. The magnesium intake was calculated from a food frequency questionnaire. RESULTS:Serum Mg2+ and urinary EGF/creatinine were significantly lower in the CNI treated children, with significantly more CNI-treated children developing hypomagnesaemia. In the latter patients, the fractional excretion of magnesium (FE Mg2+) was significantly higher. Urinary EGF, age, renal function, and serum magnesium were independent predictors of the FE Mg2+. Only 29% of the children reached the recommended daily intake of magnesium. The magnesium intake did not differ between hypomagnesemic and normomagnesemic patients and was not a predictor of the FE Mg2+. CONCLUSIONS:In CNI-treated children who developed hypomagnesemia, the FE Mg2+ was increased. The urinary EGF concentration, age, and renal function are independent predictors of the FE Mg2+.
journal_name
Nutrientsjournal_title
Nutrientsauthors
Ledeganck KJ,Anné C,De Monie A,Meybosch S,Verpooten GA,Vinckx M,Van Hoeck K,Van Eyck A,De Winter BY,Trouet Ddoi
10.3390/nu10060677subject
Has Abstractpub_date
2018-05-27 00:00:00issue
6issn
2072-6643pii
nu10060677journal_volume
10pub_type
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