Evaluation and Treatment of Disorders of Magnesium Balance
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Pediatric Nephrology (BP Dixon and E Nehus, Section Editors)
Evaluation and Treatment of Disorders of Magnesium Balance Adam R. Weinstein, MD Address 1 Geisel School of Medicine at Dartmouth, Hanover, USA Department of Pediatrics, 1 Medical Center Drive, Lebanon, NH, 03756, USA Email: [email protected]
* Springer Nature Switzerland AG 2020
This article is part of the Topical Collection on Pediatric Nephrology Keywords Hypomagnesemia I Hypermagnesuria I Hypermagnesemia I Renal magnesium wasting
Abstract Purpose of review Disorders of magnesium are reasonably prevalent, yet under-identified. We review how the kidney and gastrointestinal tract maintain normal magnesium homeostasis and the contexts and illness that may disrupt magnesium balance. We also suggest an approach to the evaluation, diagnosis, and management of magnesium disorders, with an emphasis on genetic etiologies that have helped to elucidate normal renal homeostatic functions and reveal mechanisms of disease. Recent findings Research is ongoing and continues to reveal new mechanisms of gastrointestinal and renal magnesium transport and regulation. We discuss some of the more recently identified genetic mechanisms of renal magnesium wasting and dysregulation. Summary Magnesium is an essential cation, needed for hundreds of cellular functions. Magnesium disorders may be due to either altered intake or gastrointestinal magnesium absorption or impairment of renal tubular magnesium handling. Recognizing the symptoms, risks, and co-morbidities for disorders of magnesium may help identify, diagnose, and manage groups of patients with increased hospital morbidity and mortality. Research continues to explore and clarify our understanding of mechanisms for the regulation of the total body and plasma magnesium. Additional clinical research is needed to link therapy and treatment goals with clinical outcomes.
Introduction Magnesium is the second most abundant intracellular cation after potassium. It is an essential cofactor in hundreds of cellular enzymatic processes and transport
steps, including the function of the Na/K ATPase. Disorders of magnesium present clinically with neuromuscular symptoms, such as weakness, hypotonia, tetany,
Pediatric Nephrology (BP Dixon and E Nehus, Section Editors) hyperreflexia, seizures, mental status change, and arrhythmia. Chronic hypomagnesemia can lead to kidney stone formation. Urine magnesium enhances the solubility of many stone-forming elements; therefore, magnesium deficiency, when also associated with low urine magnesium, is a risk factor for nephrolithiasis. Additionally, severe persistent hypomagnesemia decreases parathyroid hormone (PTH) secretion and PTH effect. This may lead to hypercalciuria and risk for kidney stones [1]. Magnesium deficiency is common in oncology patients and in critical illness and has been associated with increased morbidity and mortality in hospitalized patients [1, 2]. Hypomagnesemia is associated with hypokalemia and hypocalcemia. Both intracellular and extracellula
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