Intravesical bacillus Calmette–Guérin (BCG) instillation is an adjuvant treatment for non–muscle-invasive urinary bladder cancer. Although most complications associated with BCG immunotherapy are mild and self-limiting, rare albeit serious complications have been reported. Only a few cases of BCG-related rhabdomyolysis have been reported. In this study, we present the case of a 72-year-old woman who developed severe weakness and hyperCKemia following intravesical BCG instillation. A muscle biopsy was performed, and a diagnosis of drug-induced myopathy was made.
Amlodipine, a calcium channel blocker of the dihydropyridine group, is commonly used in management of hypertension, angina, and myocardial infarction. Amlodipine overdose, characterized by severe hypotension, arrythmias, and pulmonary edema, has seldom been reported in Korean literature. We report on a fatal case of amlodipine intoxication with complications including rhabdomyolysis and oliguric acute kidney injury. A 70-year-old woman with a medical history of hypertension was presented at the author's hospital 6 hours after ingestion of 50 amlodipine (norvasc) tablets (total dosage 250 mg) in an attempted suicide. Her laboratory tests showed a serum creatinine level of 2.5 mg/dL, with elevated serum creatine phosphokinase and myoglobin. The patient was initially treated with fluids, alkali, calcium gluconate, glucagon, and vasopressors without a hemodynamic effect. High-dose insulin therapy was also started with a bolus injection of regular insulin (RI), followed by continuous infusion of RI and 50% dextrose with water. Despite intensive treatment including insulin therapy, inotropics, mechanical ventilation, and continuous venovenous hemodiafiltration, the patient died of refractory shock and cardiac arrest with no signs of renal recovery 116 hours after her hospital admission.
Hyponatremia, the most common electrolyte disorder, has been rarely reported as causing rhabdomyolysis. Osmotic demyelination syndrome (ODS), a demyelinating disease of the central pons and/or other areas of the brain, is infrequently reported as associated with rapid correction of hyponatremia. This paper reports a case of ODS after correction of severe hyponatremia complicated by rhabdomyolysis. A 47-year-old female with a history of chronic alcoholism presented herself at the hospital with altered consciousness after three days of nausea and vomiting. She was on a thiazide diuretic for essential hypertension. Her blood tests upon her hospital admission showed hyponatremia (Na+ 98 mEq/L), hypokalemia (K+ 3.0 mEq/L), and elevation of her serum creatine phosphokinase (3,370 IU/L) with an increase in her serum myoglobin level 11,267 ng/mL). She was treated with intravenous fluid therapy that included isotonic and hypertonic salines along with potassium chloride. She became more alert, and her neurological condition gradually improved after the first five days of her therapy. On the ninth day after her admission, she developed progressive quadiaresis associated with dysarthria, dysphagia, and dystonia despite the resolution of her hyponatremia. Magnetic resonance imaging of her brain on 16th day revealed symmetrical areas of signal hyperintensity in her central pons, basal ganglia, and precentral gyrus in T2-weighted images, which are consistent with ODS. Her neurological symptoms steadily improved after six weeks with only supportive treatment and rehabilitation.
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Severe hyponatremia and seizures after bowel preparation with low-volume polyethylene glycol plus ascorbic acid solution Jae Young Lee, Byung Ik Jang, Yoon Jeong Nam, Jay Song, Min Cheol Kim, Seung Min Chung, Jong Geol Jang, Jae Ho Cho Yeungnam University Journal of Medicine.2015; 32(1): 55. CrossRef
Systemic capillary leak syndrome (SCLS) is an unusual entity characterized by hypovolemic shock, hemoconcentration, and hypo-albuminemia associated with paraproteinemia as a result of marked capillary hyperpermeability. Complications of this syndrome can include compartment syndromes, pulmonary edema, thrombosis, and acute kidney injury. This paper reports a case of severe SCLS accompanied by acute tubular necrosis caused by hypoperfusion and myoglobinuria secondary to rhabdomyolysis, which resulted in chronic kidney disease that necessitated hemodialysis. However, there have been rare data of residual end-organ damage after acute attacks in Korea. Therefore, this paper reports a case of complicated SCLS enough to hemodialysis and that developed into chronic kidney disease.
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Fatal Systemic Capillary Leak Syndrome after SARS-CoV-2Vaccination in Patient with Multiple Myeloma Gwang-Jun Choi, Seon Ha Baek, Junmo Kim, Jung Ho Kim, Geun-Yong Kwon, Dong Keun Kim, Yeon Haw Jung, Sejoong Kim Emerging Infectious Diseases.2021; 27(11): 2973. CrossRef
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Primary aldosteronism is characterized by hypertension, hypokalemia, and metabolic alkalosis, associated with excessive aldosterone production and suppressed plasma renin activity. Hypokalemia-induced rhabdomyolysis has been rarely reported in primary aldosteronism patients. This paper reports a case of primary aldosteronism presented with rhabdomyolysis due to severe hypokalemia. A 48-year-old male with a three-year history of hypertension presented himself at the authors' hospital with generalized weakness and myalgia in both legs over a period of several days. His laboratory findings showed hypokalemia (1.8 mEq/L) with elevations of his serum creatine phosphokinase and serum myoglobin. His plasma aldosterone level was also elevated, and his plasma renin activity was reduced. An abdominal computed tomography revealed a 2.0 cm hypodense mass in the left adrenal gland, which suggested adrenal adenoma. The accordingly underwent laparoscopic adrenalectomy. Three months later, his plasma potassium level and blood pressure became normal without the use of medications.
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Primary Aldosteronism Presenting as Hypokalemia and Rhabdomyolysis Kee Hong Park, Soo-Kyung Kim, Eun Bin Cho, Heejeong Jeong, Nack-Cheon Choi, Oh-Young Kwon, Byeong Hoon Lim, Jong Ryeal Hahm, Ki-Jong Park Korean Journal of Clinical Neurophysiology.2016; 18(1): 21. CrossRef
A 48-year-old male visited the emergency room of the authors' hospital due to nausea, vomiting, and myalgia for four days. Acute hepatitis A was identified from the serologic marker of the hepatitis A virus. Mild elevation of the serum creatinine and creatinine phosphokinase (CPK) suggested rhabomyolysis, which was confirmed with the serum aldolase, myoglobin, and urine myoglobin. With supportive care, both the liver and renal functions were recovered gradually and fully. This case shows that rhabdomyolysis can be one of the mechanisms of renal complication in cases of acute symptomatic hepatitis A.
Leptospirosis is a spirochetal infectious disease caused by Leptospira interrogans, and may vary in degree from an asymptomatic infection to a severe and fatal illness. The kidney is one of the principal target organs of Leptospira. Renal disorders caused by Leptospira infection vary from an abnormality in urinalysis to acute kidney injury (AKI). Incidence of AKI in severe leptospirosis varies from 40% to 60%. AKI reflects the severity of leptospirosis and is generally accompanied by cholestatic jaundice. The pathophysiology of AKI in leptospirosis consists of hypovolemia, direct tubular toxicity, and rhabdomyolysis. Most patients with acute leptospirosis experience severe myalgias, and show laboratory evidence of mild rhabdomyolysis. However, occurrence of severe rhabdomyolysis is rare. We report here on a patient with leoptospirosis, who had severe rhabdomyolysis and acute kidney injury without jaundice.