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+.
Highlights
Magnesium (Mg2+ ) is an intracellular cation with roles in multiple physiologic processes, such as parathyroid metabolism, cardiovascular tone, nerve conduction, and the proper function of adenosine triphosphate complexes [1]
We aimed to investigate if children who were treated with calcineurin inhibitor (CNI) developed hypomagnesemia and/or renal Mg2+ loss, and if the urinary epidermal growth factor (EGF) expression level is related to the fractional excretion of Mg2+ (FE Mg2+ )
Mg2+ was increased in patients treated with calcineurin inhibitors; (3) The urinary EGF concentration and the FE Mg2+ were inversely correlated in all research groups; (4) We defined a predictive model for the FE Mg2+ in children, including the urinary EGF concentration, age, renal function, and the serum magnesium concentration; (5) We found that only 29% of the children exceeded the reference daily intake (RDI) for
Summary
Magnesium (Mg2+ ) is an intracellular cation with roles in multiple physiologic processes, such as parathyroid metabolism, cardiovascular tone, nerve conduction, and the proper function of adenosine triphosphate complexes [1]. Needed for growth and metabolic needs is ensured [2] This balance requires interaction between the gut, the kidney, and the bone. 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. 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. The magnesium intake did not differ between hypomagnesemic and normomagnesemic patients and was not a predictor of the FE Mg2+
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