Longitudinal Study of the Role of Epidermal Growth Factor on the Fractional Excretion of Magnesium in Children: Effect of Calcineurin Inhibitors.

Kristien Ledeganck,Koen Van Hoeck,Amandine De Monie,Marleen Vinckx,Benedicte De Winter,Sarang Meybosch,Annelies Van Eyck,Charlotte Anné,Gert Verpooten,Dominique Trouet

doi:10.3390/nu10060677

Kristien Ledeganck, Koen Van Hoeck + Show 8 more

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https://doi.org/10.3390/nu10060677

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Journal: Nutrients	Publication Date: May 27, 2018
Citations: 9	License type: CC BY 4.0

Affiliation: University of Antwerp, Antwerp University Hospital

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

Introduction

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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