Posterior Reversible Encephalopathy Syndrome Induced by Hypomagnesemia due to Clostridium Difficile in a Patient with Kidney Transplant

Hypomagnesemia is found in 12% of hospitalized patients and up to 60% of intensive care unit patients and is associated with a variety of organ dysfunction. Posterior reversible encephalopathy syndrome is a neurologic hyperperfusion disorder that mostly affects posterior portions of the brain. Various theories were proposed to explain whether hypomagnesemia is etiology or associated with posterior reversible encephalopathy syndrome (PRES). A patient with kidney transplantation suffered from fatigue and reduced urine output due to chronic diarrhea induced by Clostridium difficile. Hypoparathyroidism in addition to persistent hypocalcemia and hypokalemia was observed and suggested magnesium depletion with normal serum levels. Thereafter, the status was complicated with delirium, seizures, and coma. Neurological status rapidly improved after adding intravenous magnesium sulfate to antiepileptic drugs. The second magnetic resonance imaging (MRI) showed vasogenic edema compatible with posterior reversible encephalopathy syndrome. Therefore, magnesium depletion, with normal serum levels, was considered the most implicated etiology of the syndrome in this patient. Also, hypomagnesemia during the acute phase of the syndrome and excluding all other etiology support this theory. Our case highlights hypomagnesemia-induced PRES, despite the normal serum level. Serum magnesium dropped during the acute phase of PRES, and magnesium should be maintained at the high normal limit, regardless of normal serum level. MRI findings might present after few days of symptoms; this might delay appropriate treatment.