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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2011  |  Volume : 22  |  Issue : 5  |  Page : 1037-1038
Hypernatremia due to rhabdomyolysis in a patient on statin

1 Institute of Cardiovascular Diseases, Madras Medical Mission, Chennai, India
2 Chennai Transplant Centre, Madras Medical Mission, Chennai, India

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Date of Web Publication6-Sep-2011

How to cite this article:
Victor SM, Gnanaraj A, Abraham G, Sankardas MA. Hypernatremia due to rhabdomyolysis in a patient on statin. Saudi J Kidney Dis Transpl 2011;22:1037-8

How to cite this URL:
Victor SM, Gnanaraj A, Abraham G, Sankardas MA. Hypernatremia due to rhabdomyolysis in a patient on statin. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2022 May 23];22:1037-8. Available from: https://www.sjkdt.org/text.asp?2011/22/5/1037/84563
To the Editor,

Although rhabdomyolysis with statin use is a familiar entity, [1] its occurrence in the setting of acute coronary syndrome is less well defined, in which rising muscle enzymes is often considered as a marker of myocardial infarction. We report a case of a 54-year-old man who was brought to the coronary care unit with acute left ventricular failure. He was a known diabetic and smoker, referred from another hospital for further management. He was apparently well the previous day, when he developed progressively worsening dyspnea. He was diagnosed to have acute anterior wall myocardial infarction and echocardiogram revealed severe left ventricular dysfunction. The patient was intubated and maintained on ventilator support. He developed ventricular tachycardia and was cardioverted once. Successful percutaneous tansluminal coronary angioplasty (PTCA) to the left anterior descending (LAD) artery was performed and an intra-aortic balloon pulsation catheter was inserted. Gradually, he was weaned off the ionotropic support and was extubated. His CK and CK-MB showed a downward trend for the next four days [Table 1]. However, the patient's oxygen saturations dropped and he had to be reintubated. A profile of cardiac enzymes showed rising CK and CK-MB fraction and his troponins remained elevated, but almost static. Initially, he was thought to be having an ongoing ischemia and his medications were optimized. During this period, he had persistent hypernatremia (ranging from 153 to 159 mEq/L), which was only partially corrected with free water. Serum CK levels were 21,025 U/L and MB was 300 U/L. A diagnosis of rhabdomyolysis was considered after excluding the other causes of hypernatremia and atorvastatin 40 mg, which he received for nearly two weeks, was stopped immediately. Over the next two days, the patient developed significant elevation of renal parameters, myoglobin levels and hyperkalemia. He voided port-wine-colored urine. His liver function and coagulation profile were not significantly altered. In spite of treatment, his renal parameters continued to rise and his urine output reduced. Peritoneal dialysis was planned but the patient's hemodynamics worsened and he had a cardiac arrest and could not be revived.
Table 1: Laboratory values of the patient in a chronological order.

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Rhabdomyolysis may range from subclinical rise of CK to life-threatening acute renal failure. A frequent cause of drug-induced rhabdomyolysis today is the administration of HMG-CoA reductase inhibitors, [2] which are one of the most important cardiac drugs in the treatment of acute coronary syndrome due to their pleiotropic effects.

CK, which is present in both striated and cardiac muscle, rises to considerable levels in rhabdomyolysis up to 100,000 IU/mL. [2] Elevations in CK are conventionally used in the diagnosis of both rhabdomyolysis and acute coronary syndrome along with the other markers, and may cause a diagnostic confusion when both the conditions co-exist. Hypernatremia in rhabdomyolysis is reported to be associated as both cause and effect. [3],[4],[5] In our patient, although the Na+ levels elevations were only moderate, the pattern of persistent hypernatremia with elevated CK raised the suspicion of rhabdomyolysis in spite of the absence of other clinical features, electrolyte derangement and only minimal rise in creatinine levels initially.

The persistent hypernatremia caused by rhabdomyolysis guided us to the correct diagnosis.

The hypernatremia in this setting should not be treated with free water as in the usual case of hypernatremia, and dialysis would be the more appropriate method of treatment.

   References Top

1.Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review: Rhabdomyolysis: an overview for clinicians. Crit Care 2005;9:158-69.  Back to cited text no. 1
2.Vanholder R, Sever MS, Erek E, Lameire N. Rhabdomyolysis. J Am Soc Nephrol 2000;11: 1553-61.  Back to cited text no. 2
3.Asahara H, Maruyama S, Tamura K, Miyoshi T. A case of severe hypernatremia complicated with rhabdomyolysis. Department of Neurology, Kyushu Rosai Hospital. Rinsho Shinkeigaku 1998;38(4):301-4.  Back to cited text no. 3
4.Incecik F, Herguner OM, Yildizdas D, Ozcan K, Altunbasak S. Rhabdomyolysis caused by hypernatremia. Indian J Paediatr 2006;73(12): 1124-6 .  Back to cited text no. 4
5.Walter LA, Catenacci MH. Rhabdomyolysis. Hospital Physician. January 2008;44(1)25-31.  Back to cited text no. 5

Correspondence Address:
Suma M Victor
Institute of Cardiovascular Diseases, Madras Medical Mission, Chennai
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Source of Support: None, Conflict of Interest: None

PMID: 21912045

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