Renal magnesium wasting and hypomagnesemia are common in transplant patients. Hypomagnesemia may be caused by poor dietary intake (malnutrition, alcoholism), malabsorption from the GI tract (diarrhea, malabsorption syndrome) and increased magnesium losses in the urine (cyclosporine, tacrolimus, diuretics, aminoglycoside antibiotics, and amphotericin B).

Table 17.3. Therapeutic approach to severe hyperkalemia



Peak Effect

Calcium Gluconate* Insulin and Glucose*

Sodium Bicarbonate




10-30 ml of 10% solution Insulin, 5 U IB bolus, followed by Bw/min in 50 ml of 20% glucose 100 ml 1.4% solution 2 mmol/min 20 mg in the nebulized form Enema (50-100 g) Oral (40g)

Variable 1-6 h 60 min 2-4 h

30-60 min

*Denotes recommended initial therapy.

Hemodialysis is not listed as immediate therapy since it is usually not available within the first hour or so of arrival to the hospital. If available, it could replace insulin therapy. Adapted from Rombola G. Batlle DC; Hyperkalemia, P. 49. In Jacobson H. Stricker G. Hklar S et al (eds):

Principles and practice of Nephrology. BC Decker. Philadelphia. 1990. With permission.

Clinical manifestations of hypomagnesemia are generally not seen until serum magnesium level are less than 1mg/dl, and may include: lethargy, confusion, tremor, positive Trousseau's and Chvostek's signs, muscle fasciculations, ataxia, nystagmus, tetany and seizures. EKG abnormalities include prolonged PR and QT intervals. Atrial and ventricular arrhythmias may occur, especially in patients receiving Digoxin.

Treatment of hypomagnesemia must be given with extreme care in patients with impaired kidney function because of the risk of causing hypermagnesemia. For severe symptomatic hypomagnesemia serum magnesium level (< 1mg/dl) see Table 17.4. Correct mild or chronic hypomagnesemia with Mag-Ox 400 mg tablets (contains 240 mg of elemental magnesium) q.d.-b.i.d. The major side effect of Mag-Oxide tablets is diarrhea.

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