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Hypomagnesemia is not a typical concern in patients with stage 5 chronic kidney disease. Magnesium (Mg) is cleared renally, so Mg concentration is usually normal or even elevated in patients with chronic kidney disease. Up to 95% of renally filtered Mg can be reabsorbed in the nephron. Certain medications, such as diuretics (loop, thiazide, and osmotic), cisplatin, gentamicin, and s-lactam antibiotics, increase Mg excretion. The gastrointestinal absorption of Mg is dose-dependent and occurs by paracellular uptake at high Mg concentrations and by active transport at low Mg concentrations. Depending on the salt form, 30%–50% of ingested Mg is absorbed. Certain gastrointestinal disorders cause malabsorption, and certain medications, such as proton-pump inhibitors, reduce absorption, either of which can lead to hypomagnesemia. Renal dysfunction can lead to hypermagnesemia, yet gastrointestinal malabsorption can lead to hypomagnesemia; when these 2 conditions occur concurrently the change in serum magnesium is unpredictable. The clinical signs of hypomagnesemia range from fatigue, anemia, and hypokalemia to neuromuscular instability characterized by ataxia, vertigo, and hyperreflexia. Mild hypomagnesemia can be corrected by oral supplementation, with or without coadministration of vitamin D or a vitamin D analogue. In more severe cases, parenteral administration of magnesium sulphate is often required, most commonly by IV administration; however, in some cases, intraperitoneal (IP) administration of Mg has been successful in correcting hypomagnesemia. This report describes a patient with stage 5 chronic kidney disease whose hypomagnesemia was corrected by IP administration of magnesium sulphate.

Intermittent Intraperitoneal Administration of Magnesium Sulphate in an Elderly Patient Undergoing Dialysis