Anita C. Truttmann

Maintenance Hemodialysis and Circulating Ionized Magnesium

Background: Circulating magnesium exists in the bound and in the free ionized form, that is biologically active. In kidney disease the relationship between ionized and total circulating magnesium is often altered. Little information is available on the influence of hemodialysis on the relationship between ionized and total circulating magnesium in end-stage kidney disease. Methods: Plasma total and ionized magnesium and the plasma ionized magnesium fraction were assessed before and after hemodialysis (dialysate magnesium content 0.75 mmol/l) in 46 patients with end-stage kidney disease and in a control group of 25 healthy subjects. Results: In patients plasma total (from 1.19 [1.05–1.33] to 1.10 [1.02–1.16] mmol/l; median and interquartile range) and ionized (from 0.71 [0.66–0.78] to 0.65 [0.63–0.69] mmol/l) magnesium significantly decreased during dialysis (control subjects: 0.82 [0.80–0.92], respectively, 0.57 [0.54–0.59] mmol/l). The plasma ionized magnesium fraction was significantly lower in patients both before (0.61 [0.58–0.64)] and after (0.60 [0.56–0.62]) hemodialysis than in controls (0.68 [0.65–0.70]). Conclusion: The study demonstrates a tendency towards a reduced circulating ionized magnesium fraction in end-stage kidney disease that is not corrected by hemodialysis.

Circulating Ionized and Total Magnesium in End-Stage Kidney Disease

Background: Circulating magnesium exists in the ionized state and in the undissociated form, either bound to albumin, or complexed to various anions. Until recently, only the measurement of total plasma magnesium has been possible. Now circulating ionized magnesium can be assessed as well. Methods: Total and ionized plasma magnesium were determined in 43 patients on maintenance hemodialysis (dialysate composition: calcium 1.75 mmol/l, magnesium 0.75 mmol/l) before a dialysis session and in a group of 23 healthy subjects. Results: The total (1.16 [1.03–1.31] versus 0.81 [0.78–0.89] mmol/l; median and interquartile range) and the ionized (0.71 [0.66–0.78] versus 0.54 [0.53–0.59] mmol/l) plasma magnesium levels were significantly higher (p < 0.01) and the ionized plasma magnesium fraction lower (0.61 [0.58–0.65] versus 0.67 [0.64–0.70]; p < 0.02) in patients than in controls. Conclusion: The determination of circulating ionized magnesium using selective electrodes is an attractive method to evaluate extracellular magnesium in kidney disease.

Free Circulating Magnesium and Renal Magnesium Handling during Acute Metabolic Acidosis in Humans

Ion-selective electrodes have been designed for determining the ionized concentration of magnesium in blood, the biologically active form of this ion. The effect of acute acidosis induced by ammonium loading on circulating and urinary magnesium was investigated in 11 volunteers. No changes in plasma total and ionized magnesium were noted following administration of ammonium chloride. On the contrary, administration of ammonium chloride increased the plasma free magnesium fraction and the urinary magnesium excretion. The study demonstrates that the hypermagnesiuria induced by acute acidosis is not caused by ionized hypermagnesemia and supports the theory that acidosis decreases the circulating magnesium fraction that is bound to proteins.

PLASMA-IONIZED MAGNESIUM CONCENTRATION IN A CHILD WITH MAGNESIUM-LOSING TUBULOPATHY

Dr. M.G. Bianchetti, Inselspital, CH-3010 Berne (Switzerland) Dear Sir, Circulating magnesium [1], like calcium [2], exists in the ionized state and in the undissociated form, either bound to proteins, primarily albumin, or complexed to anions like bicarbonate, citrate, and phosphate. Technology for detecting circulating ionized magnesium, the most interesting form with respect to physiological and biological properties, is now available via the new magnesium-selective electrodes [3]. It has been suggested that the circulating ionized magnesium approximates 55-65% of the total magnesium [1]. However, it is tempting to assume that the total and free concentrations of magnesium often do not go hand in hand [1]. For this reason we recently assessed total and free concentration of magnesium in a patient with hereditary magnesium-losing tubulopathy [4, 5]. On September 21, 1994, a 3-year-old girl was referred to us with a 2-day history of abdominal pain and vomiting. She had had a febrile convulsion at the age of 9 months. The girl appeared moderately dehydrated. The blood chemistry revealed severe hypo-kalemia (1.9mmol/l), hypochloremia (79.0 mmol/l), and metabolic alkalosis (venous blood pH 7.454, plasma bicarbonate 33.1 mmol/l). Blood urea (3.70 mmol/l), creati-nine (41 μmol/l) and albumin (39 g/l) were within normal ranges. The laboratory findings failed to normalize in spite of parenteral rehydration with normosaline and supplementation with potassium chloride 5 mmol/ kg daily. Subsequently, abnormal urinary chloride (molar chloride to creatinine ratio 27.5) and magnesium (molar magnesium to creatinine ratio 1.28) excretion were demonstrated in the girl, despite a pathologically reduced plasma chloride (89 mmol/l) and total magnesium concentrations (0.43 mmol/ 1). The molar urinary calcium to creatinine ratio was 0.081, thus clearly less than 0.200 [5]. These laboratory findings were therefore considered characteristic for Gitelman syndrome, the hypocalciuric variant of Bartter syndrome [4, 5]. Total plasma magnesium (by the xylide blue I photometric method) Table 1. Plasma total and ionized magnesium concentrations in a girl with Gitelman syndrome and in 74 healthy subjects (38 males and 36 females, aged from 20 to 38 years)