Clinical and laboratory features of hyponatremia-induced myopathy.
BACKGROUND
The present study was undertaken to determine the clinical and laboratory features of hyponatremia-induced myopathy.


METHODS
We collected 14 hyponatremic subjects (six men and eight women) with serum creatine kinase (CK) levels of more than 500 IU/ml during the 5-year period between 2001 and 2005. The mean +/- SD patients' age was 66.5 +/- 16.7 years (range, 37 to 88 years).


RESULTS
The causes of the hyponatremia were: syndrome of inappropriate secretion of antidiuretic hormone (SIADH; n = 4), mineralocorticoid-responsive hyponatremia of the elderly (MRHE; n = 2), hypopituitarism (n = 1), psychogenic polydipsia (n = 3), congestive heart failure (n = 3), and unknown cause (n = 1). The subjects were subgrouped into two groups: acute onset of myopathy and slowly progressive onset. The age at onset was 62.0 +/- 5.7 years (mean +/- SEM) in the subjects with acute onset, and 77.8 +/- 1.5 years in those with slowly progressive onset (P = 0.02). At the onset, there was no difference in serum Na levels between the acute onset and the slowly progressive onset groups, but there was a significant difference in maximal serum CK levels between the groups (7072 +/- 2317 vs 722 +/- 104 IU/ml; P = 0.02). Maximal serum CK levels were widely distributed among the ages in the subjects with acute onset, whereas maximal serum CK levels were mildly elevated in the elderly subjects with slowly progressive onset. The elevated serum CK levels were normalized at a maximum of 14 days after the onset in all the subjects.


CONCLUSIONS
The present findings indicate that hyponatremia infrequently causes skeletal muscle disruption, and that there are two types of hyponatremia-induced myopathy, acute onset and slowly progressive onset.
Sasaki
Masami
M
Department of Medicine, Jichi Medical University Omiya Medical Center, 1-847 Amanuma, Omiya-ku, Saitama, 330-8503, Japan.
Yuzawa
Miho
M
Department of Medicine, Jichi Medical University Omiya Medical Center, 1-847 Amanuma, Omiya-ku, Saitama, 330-8503, Japan.
Saito
Tomoyuki
T
Department of Medicine, Jichi Medical University Omiya Medical Center, 1-847 Amanuma, Omiya-ku, Saitama, 330-8503, Japan.
Ikoma
Aki
A
Department of Medicine, Jichi Medical University Omiya Medical Center, 1-847 Amanuma, Omiya-ku, Saitama, 330-8503, Japan.
Tamemoto
Hiroyuki
H
Department of Medicine, Jichi Medical University Omiya Medical Center, 1-847 Amanuma, Omiya-ku, Saitama, 330-8503, Japan.
Kawakami
Masanobu
M
Department of Medicine, Jichi Medical University Omiya Medical Center, 1-847 Amanuma, Omiya-ku, Saitama, 330-8503, Japan.
Ishikawa
San-E
SE
Department of Medicine, Jichi Medical University Omiya Medical Center, 1-847 Amanuma, Omiya-ku, Saitama, 330-8503, Japan. saneiskw@jichi.ac.jp.
D000208:Acute Disease; D000328:Adult; D017668:Age of Onset; D000368:Aged; D000369:Aged, 80 and over; D003402:Creatine Kinase / Q000097:blood*; D018450:Disease Progression; D005260:Female; D006801:Humans; D007010:Hyponatremia / Q000097:blood / Q000150:complications* / Q000209:etiology; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000201:enzymology*; D009135:Muscular Diseases / Q000097:blood* / Q000145:classification / Q000453:epidemiology / Q000209:etiology; D012720:Severity of Illness Index; D012964:Sodium / Q000097:blood*
D012964:Sodium; D003402:Creatine Kinase