Refractory Acute Kidney Injury Secondary to Hypothyroid-Induced Myopathy: A Contemporary Case Report

Phillip Ulyanovskiy, Deborah Dergan, Shams Abbas, Prabhjot Manes, Irina Erlikh


This is a case report elucidating how severe hypothyroid-induced myopathy can lead to refractory kidney injury, unmanageable by standard medical and hemodialysis interventions. A 70-year-old female with extensive medical comorbidities including adult onset hypothyroidism, hypertension, hyperlipidemia, and normal baseline renal function presented with shortness of breath, myalgias, edema, and facial swelling. The patient was found to have a thyroid-stimulating hormone of 169.8 uIU/mL, creatine phosphokinase of 42,670 U/L, blood urea nitrogen of 70 mg/dL, a creatinine of 12.1 mg/dL, and glomerular filtration rate of 3 mL/min/1.73 m2. She was initiated on aggressive intravenous isotonic rehydration, along with intensive intravenous thyroid hormone replacement therapy and hydrocortisone treatment as well. Her renal status failed to improve adequately and she was started on sodium bicarbonate for urinary alkalinization. With the preceding interventions deemed medically futile for renal amelioration, the patient was started on acute hemodialysis. Over the course of 2 weeks and six hemodialysis treatments, the patient’s renal status failed to improve. The patient finally refused any further hemodialysis or medical interventions seeing that her kidneys failed to respond to treatment, and her clinical prognosis remained poor. This case report illustrates how severe symptomatic hypothyroidism can induce rhabdomyolysis leading to intractable kidney failure, unmanageable by standard medical therapy and hemodialysis.

J Med Cases. 2017;8(1):8-10



Hypothyroidism; Hypothyroid-induced myopathy; Rhabdomyolysis; Acute kidney injury; Acute renal failure; Acute hemodialysis; Thyroid hormone; Thyroid hormone replacement therapy

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