Measuring magnesium – Physiological, clinical and analytical perspectives Original paper

What was reviewed?

This paper reviewed magnesium biology and the practical clinical question of how to measure magnesium well enough to guide care. The authors connected basic physiology (absorption in the gut, storage in bone and muscle, and kidney control of excretion) to real-world lab testing, and they compared common measurement approaches in blood and urine. They also reviewed how medications and disease states drive magnesium imbalance, why these abnormalities often get missed in hospitalized patients, and what analytical issues (sample type, method bias, interference, and lack of standardization) can distort results and clinical decisions.

Who was reviewed?

The paper did not study a single patient cohort. Instead, it synthesized prior human clinical studies, laboratory method evaluations, and guideline-style evidence spanning healthy adults and pediatric reference interval work, critically ill and surgical patients, kidney and transplant populations, and patients exposed to magnesium-altering drugs. The “who” therefore includes the broad clinical populations represented across the cited literature, rather than a defined group enrolled by the authors.

What were the most important findings?

The most actionable finding is that “total serum magnesium” can misclassify status, especially in critical illness, because it includes protein- and ligand-bound magnesium and may not track the physiologically active fraction. The review emphasizes that free (often called “ionized”) magnesium may better reflect biologic activity, but it remains uncommon due to electrode selectivity issues, pH effects, and limited standardization and reference ranges. The authors also highlight urine magnesium as a powerful tool when interpreted correctly: spot urine magnesium normalized to creatinine and the fractional excretion of magnesium can help distinguish renal magnesium wasting from low intake or gastrointestinal loss. Method choice matters because dye-binding assays dominate routine testing but can suffer from interferences and calibration differences, while enzymatic approaches can offer better selectivity yet still show variability across platforms. For microbiome context, the review supports that intestinal absorption depends on intake and transport pathways (notably TRPM6/7), but it does not report microbial signatures or consistent organism-level associations.

What are the greatest implications of this review?

Clinicians should treat magnesium as a high-impact electrolyte, not a “background lab,” because abnormal levels can worsen outcomes and can be drug-driven, preventable, and clinically silent until severe. This review supports a more targeted strategy: interpret magnesium using the right specimen and method for the clinical question, consider urine-based indices when etiology is unclear, and recognize that a “normal” total magnesium may not rule out functionally important deficiency in high-risk settings. It also implies that health systems could improve care by standardizing measurement practices, validating decision cutoffs locally, and expanding access to reliable free magnesium testing where it changes management.