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Letter to the Editor

Nephron 1995:71:477-478

Hidenori Matsuoa
Kazunori Nakamurab
A Case of Hypermagnesemia
Akira Nishidab
Kazuo Kubob
Accompanied by Hypercalcemia
Ryohichi Nakagawac
Yukiharu Sumidac
Induced by a Magnesium Laxative
Dialysis Center. Hidaka Hospital, Takasaki, in a Hemodialysis Patient
Department o f Nephrology, Tokyo
Women’s Medical College, and
Kita Hospital, Tokyo, Japan

Dear Sir,
It is understood that hypermagnesemia was 216/104 mm Hg. Pulse rate was 80, reg­ Serum calcium elevation appeared to oc­
can occur in patients with chronic renal fail­ ular and full. The E C G showed a regular si­ cur simultaneously with that o f magnesium.
ure during the administration o f magnesium nus rhythm. The blood chemistry revealed a This implies that the administration o f mag­
even at a pharmacological dose. According marked elevation o f serum magnesium up to nesium might have played a role as a trigger
to previous reports about hypermagnesemia, 9.9 mg/dl. This was on the 35th day, since to elevate the serum calcium level. This phe­
which the authors could refer to, the serum magnesium administration was begun. We nomenon can happen, as many authors have
calcium level o f those patients was decreased decided to start dialyzing every day. His already described, in cases o f hypocalcémie
or unchanged [ 1 . 2 ], state o f consciousness improved on the 4th and hypomagnesemic states, in which not
We report our experience with a case o f day. Intermittent hemodialysis was per­ only the supplementation o f calcium and
hypermagnesemia accompanied by hyper­ formed every day until the 23rd hospital vitamin D 3, but also the administration o f
calcemia induced by a magnesium laxative, day, when the serum magnesium level re­ magnesium are necessary for restoring the
which occurred in a hemodialysis patient. A turned to normal. serum calcium level [3-5], To our regret, we
63-year-old male was transferred to the Kita Looking back over the course o f the 231 failed to evaluate the serum P T H level or
Hospital from a dialysis clinic because o f days (see fig. 1), from 77 days before until l,25-(OH)2 vitamin D . O ur patient was
neurological changes. He suffered from 154 days after this patient received magne­ probably in a hyperparathyroid state, con­
chronic renal failure and anuria due to sium, at what drugs were taken, how many sidering the high level o f serum alkaline
chronic glomerulonephritis, having received times dialysis was received, and the blood phosphatase, which was about 2- to 5-fold
hemodialysis for 7 years. The patients had chemistry o f the patient, we noticed the fol­ above the normal value, and not in a hypo-
had occasional episodes o f obstipation. 6 lowing. (1) Serum total magnesium, which parathyroid state. After the administration
weeks previously, he had complained o f a had been at the level o f 2.6-3.3 mg/dl pre­ o f magnesium, the parathyroid function
sense o f fullness, loss o f appetite, and no pas­ viously, began to increase 2 weeks after the might have been suppressed, and serum al­
sage for 10 days. Magnesium oxide powder initiation o f the administration, and total kaline phosphatase become low. On the oth­
was administered at 3.0 g/day. since differ­ calcium, 8.5-9.9 mg/dl initially, also began er hand, he was not obviously hypomagne­
ent purgatives tried up to then had failed to to increase parallel with magnesium, reach­ semic initially. However, it could be possible
improve his complaint. A few days later, he ing its peak serum level o f 13.5 mg/dl. (2) A that the intracellular magnesium level had
had a passage every day, and his appetite remarkable decrease o f the serum phosphate actually been low, as Lim et al. [6] had
improved. In the 4th week, however, he level (7.9 mg/dl initially to 1.7 mg/dl 28 days described, and changing o f serum magne­
began to manifest vomiting, became irrita­ after administration) and alkaline phospha­ sium to a higher level, by adding large
ble, confused, and disoriented regarding tase level (from 176 to 42 Babson units/1 105 amounts o f magnesium oxide powder, might
time and surroundings. days after administration) occurred after ad­ have been activated the pharmacological ef­
On admission, he was o f medium stature ministering magnesium. (3) During the over­ fect o f la-(OH) vitamin D 3 on calcium me­
for a Japanese male: 160 cm in height, all course, la (O H )D 3(la-hydroxycholecalci- tabolism. resulting in hypercalcemia. This
weighing 54 kg. His state o f consciousness ferol) was administered at the dose o f 1.5 pg/ case suggests that some mechanisms exist in
was stuporous. However, deep tendon re­ day. (4) There was no administration o f cal­ magnesium-calcium metabolism, which are
flexes were present and the respiratory cium salts. not well defined yet.
movement was not impaired. Blood pressure

Hidenori Matsuo. M D © 1995 S. Karger A G . Basel


Hidaka Hospital 0028-2766/95/0714-0477
886 Nakao machi S 8.00/0
Takasaki. Gunm a 370 (Japan)
0 I t ............... r f n -T T T I ' i i
-100 -5 0 50 100 150 200 days
Fig. 1. Medications given to this patient,
including the dialysis sessions and drugs. All MgO 3 g daily

drugs were administered orally. Line graphs


I 01-OH-D3 1.5 jig daily
indicate changes in serum total magnesium,
total calcium, phosphate and alkaline phos­
phatase level. The alkaline phosphatase level Other drugs (daily):
sennosides 72 mg.
is given in Babson units/l. Blood chemistry dried aluminum hydroxide gel 3.0 g.
was examined approximately every 5-14 nicardipine hydrochloride 120 mg.
hydralazine hydrochloride 150 mg.
days at the initiation o f every dialysis ses­ allopurinol 200 mg
sion. H D = Hemodialysis.

Acknowledgements
References
We thank Mrs. K . Suzuki and Mr. K.
1 Fawcett D W , Gens JP : Magnesium poisoning 5 Ducreux M , Messing B, De Vemejoul M -C ,
Sukegawa, the nursing staff o f the Dialysis
following an enema o f epsom salt solution. Bouhnick Y , Milavct L , Rambaud J-C : C al­
Center o f Kita Hospital, for their collabora­ JA M A 1943:123:1023-1029. cémie response to magnesium or 1-alpha-hy-
tion. and Mrs. Johanna Matsuda for the cor­ 2 Randall R E . Cohen M D , Spray C C . Rossmeisl droxycholccalcifcrol treatment in intestinal hy­
rection o f the manuscript. EC: Hypermagnesemia in renal failure. Etiolo­ pomagnesemia. Gastroenterol Clin Biol 1991;
gy and toxic manifestations. Ann Intern Med 15:805-811.
1964;61:73-88. 6 L im P . D o n gS . K h o oO T : Intracellular magne­
3 Rosier A , Rabinowitz D : Magnesium induced sium depletion in chronic renal failure. N Engl
reversal o f vitamin D resistance in hypopara­ J Med 1969;280:981-984.
thyroidism. Lancet 1973;i:803—805.
4 Medallc R, Waterhouse C , Hahn T J: Vitamin
D resistance in magnesium deficiency. Am J
C lin Nutr 1976:29:854-858.

478 Matsuo/Nakamura/Nishida/Kubo/ A Case o f Hypermagnesemia with


Nakagawa/Sumida Hypercalcemia in a Hemodialysis Patient

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