Hypothyroidism is a rare cause of rhabdomyolysis and an even less common cause of acute kidney injury (AKI). Because the symptoms may be mild or non-specific, the diagnosis can easily be overlooked. We report the case of a 44-year-old man with no significant past medical history who was admitted after renal impairment was discovered on routine blood testing. On clinical examination, he had sinus bradycardia, puffy facies with bilateral periorbital edema, Hertoghe sign, muffled heart sounds, psychomotor slowing, and constipation. Laboratory investigations showed stage II AKI, severe rhabdomyolysis with creatine phosphokinase levels above 8,450 IU/L (reference range: <171 IU/L), and liver cytolysis. Further evaluation revealed profound hypothyroidism, with markedly elevated thyroid-stimulating hormone, very low free thyroxine, and strongly positive anti-thyroid peroxidase antibodies, consistent with autoimmune thyroiditis. Thyroid ultrasound supported the diagnosis of Hashimoto’s thyroiditis, and echocardiography showed a moderate pericardial effusion without hemodynamic compromise. Because nephrotic-range proteinuria was also present, a kidney biopsy was performed and showed mainly tubulointerstitial injury with pigmented casts and tubular atrophy, associated with focal segmental glomerulosclerosis. The patient was treated with intravenous hydration and gradual levothyroxine replacement, with clear clinical improvement and progressive normalization of laboratory abnormalities. This case highlights that severe hypothyroidism may rarely present with rhabdomyolysis and AKI. It also underlines the importance of considering thyroid dysfunction in patients with unexplained rhabdomyolysis, especially when the clinical picture is not very suggestive, since early treatment can lead to a favorable outcome.
Dadi et al. (Sat,) studied this question.
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