MON-375 - Rhabdomyolysis and Acute Kidney Injury in the Setting of Overt Hypothyroidism: An Uncommon Etiology

Background:
Rhabdomyolysis is a potentially life-threatening syndrome that may result in acute kidney injury (AKI) and electrolyte abnormalities. While commonly traumatic or toxic in origin, hypothyroidism is a rare and underrecognized metabolic cause.

Case Presentation:
A 52-year-old man with a history of hypertension and opioid use disorder was brought to the emergency department for abnormal outpatient laboratory results showing increased creatinine and hyperkalemia. He reported one week of progressive generalized edema and three weeks of weight gain, fatigue, cold intolerance, constipation, exertional dyspnea, hoarseness, and a sensation of tongue enlargement. He denied trauma, prolonged immobilization, recent illness, or recent substance use. Medications included buprenorphine-naloxone, which he had not taken for four days prior to presentation.

On examination, he was hypertensive (174/103 mmHg) but otherwise hemodynamically stable, with diffuse nonpitting edema. Laboratory evaluation revealed creatinine 2.0 mg/dL (baseline 1.1), potassium 5.6 mmol/L, and creatine kinase (CK) 4,756 U/L; Thyroid studies demonstrated severe hypothyroidism with TSH 225 µIU/mL, undetectable free T4 ( < 0.25 ng/dL), low T3 (2.21 pg/mL), and markedly elevated thyroid peroxidase antibodies (>10,000 IU/mL). Urine toxicology was positive only for buprenorphine metabolites.

The patient was treated with intravenous fluids and initiated on weight-based levothyroxine. During hospitalization, CK downtrended to 1,323 U/L with concomitant improvement in renal function.

Discussion:
Thyroid hormone deficiency disrupts skeletal muscle metabolism through impaired glycogenolysis, reduced mitochondrial oxidative capacity, and decreased myosin ATPase activity, predisposing to myocyte injury and necrosis. In the absence of alternative precipitating factors, severe hypothyroidism was the most likely etiology of this patient’s rhabdomyolysis, supported by biochemical and clinical improvement following thyroid hormone replacement.

Conclusion:
Severe hypothyroidism can directly precipitate rhabdomyolysis and secondary acute kidney injury even in the absence of trauma, immobilization, or toxic exposures. Clinicians should include thyroid function testing in the evaluation of unexplained rhabdomyolysis, as prompt initiation of thyroid hormone replacement can accelerate creatine kinase decline, improve renal function, and reduce the risk of further complications. This case suggests that untreated autoimmune hypothyroidism may present with severe systemic complications before classic thyroid disease is recognized.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*