Guidelines Supporting the use of Renamag (Mg Glycerophosphate)

The magnesium in Renamag, magnesium glycerophosphate is available as a prescription in the UK.  The UK National Health Service and Oxford University Hospitals have developed guidelines on the treatment of hypomagnesemia using magnesium glycerophosphate.

  • Grade 1:  Mild Hypomagnesemia.  1.2 – 1.7 mg/dl

    Only replace if patient is symptomatic.

    1st line oral

    Magnesium Glycerophosphate 8 mmol three times a day. (2-4 Renamag doses per day in divided doses)

    2nd line intravenous

    10 mmol magnesium sulphate in 100 ml-1L sodium chloride 0.9% or glucose 5% over 3-12 hours.

  • Grade 2: Moderate hypomagnesemia 1.0 – 1.2 mg/dl

    Either

    Oral

    Magnesium Glycerophosphate 8 mmol three times a day. (4-6 Renamag doses per day in divided doses)

    or

    Intravenous

    20 mmol magnesium sulphate in 100ml-1L sodium chloride 0.9% or glucose 5% over 3-12 hours.

  • Grade 3: Severe hypomagnesemia <1.0 mg/dl

    Intravenous

    20 mmol magnesium sulphate in 100 ml-1L sodium chloride 0.9% or glucose 5% over 3-12 hours.

Renamag Dosing Conversion

There are many factors that can affect the absorption and tolerability of various magnesium salts.  This said, below is a general conversion from magnesium oxide to Renamag/magnesium glycerophosphate.


Mg glycerophosphate bioavailability 60%

Mg oxide Bioavailability 15%


Renamag dose of two 425mg capsules = 100mg elemental Mg x 60% = 60mg Mg

Mg oxide 400 mg =244mg elemental Mg x 15% = 37mg Mg

Pediatric use dosing

Click below to link to pediatric dsoing for Mg Glycerophosphate from Leeds Teaching Hospital in the UK

Details on the above guideline

1. Introduction

Magnesium is essential for a number of intracellular functions and low levels may potentially be life-threatening. Patients within the Clinical haematology department frequently present with hypomagnesaemia and almost all patients will require magnesium replacement in the immediate post-transplant period and on-going magnesium replacement may be necessary for several weeks afterwards.

 

This guideline summaries the magnesium replacement options both oral and IV within the Adult Clinical haematology department only. The recommendations within this guideline are not intended for patients with impaired renal function; patients with impaired renal function will require dose adjustments and should be discussed with a haematology registrar on an individual basis.

See separate section for patients on pentamidine. This guideline does not cover the prescribing of magnesium for specialist uses e.g. pre-eclampsia, asthma or AF.

2. Causes of Hypomagnesaemia

Common causes of hypomagnesaemia seen in haematology patients include:

Gastrointestinal losses: vomiting, diarrhoea, malabsorption (due to mucositis or Graft versus Host Disease especially in allograft patients)Renal losses, Blood transfusion, Hypercalcaemia and hypokalaemia, Dietary deficiency and Re-feeding syndrome, Syndrome of inappropriate antidiuretic hormone secretion and Acidosis

Common causes of medically induced hypomagnesaemia seen in haematology patients include:

Cisplatin, Ciclosporin and tacrolimus, Pentamidine (see point 6), Foscarnet, Aminoglycosides, Gentamicin, Amphotericin B (Ambisome), Diuretics, Proton Pump Inhibitors.

Main Clinical ManifestationsHypomagnesaemia can cause a number of symptoms and signs, most of which are non- specific and rarely occur unless the magnesium level is less than 0.4 mmol/L. They include Neuromuscular symptoms: tremors, tetany, cramps, seizures, ataxia and muscle weakness.

H.95V.1.0.

Authorized by: Dr. Andy Peniket / Nadjoua Maouche

Department of Clinical Haematology

 

hypomagnesaemia is graded according to the National Cancer Institute-Common Terminology Criteria for Adverse Events (CTCAE), version 4, as follows:

Grade 1 – Mild

Grade 2 – Moderate
Grade 3 – Severe
Grade 4 – Life Threatening : <0.3mmol/L

Note: The majority of magnesium is stored in the bone, muscle and the liver, and it is primarily intracellular – the little that is extracellular is protein bound or ionized therefore hypoalbuminaemic states may cause levels to appear falsely low.