NutriStack
What is happening. Tenofovir disoproxil can cause proximal renal tubular dysfunction (a Fanconi-like syndrome) that produces urinary wasting of phosphate, potassium, and magnesium in susceptible patients. Low serum magnesium may develop or worsen during long-term therapy, and unrecognized hypomagnesemia can in turn make potassium and calcium repletion difficult. Magnesium glycinate is a reasonable, well-tolerated form for correcting documented deficiency, but supplementation should be guided by lab values rather than used to mask ongoing tubular injury.
Mechanism. TDF-related proximal tubulopathy impairs reabsorption of magnesium (and phosphate, potassium, bicarbonate, glucose, amino acids), leading to renal magnesium wasting. Oral magnesium repletion restores serum levels but does not reverse the underlying tubular defect.
Recommendation. If a patient on long-term TDF develops fatigue, muscle cramps, or electrolyte abnormalities, check serum magnesium, potassium, phosphate, and renal tubular markers. Replete magnesium when deficiency is confirmed; magnesium glycinate is gentler on the gut than oxide. Persistent or worsening electrolyte wasting should prompt evaluation for tenofovir nephrotoxicity and possible switch to tenofovir alafenamide. Avoid high-dose magnesium in renal impairment without monitoring.