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Kidney Week

Abstract: FR-PO229

Severe Hypothyroidism Presenting as Rhabdomyolysis and Acute Tubular Necrosis

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Aamer, Sameen, Allegheny Health Network, Pittsburgh, Pennsylvania, United States
  • Butt, Muhammad Ali, Allegheny Health Network, Pittsburgh, Pennsylvania, United States
  • Dunmyre, Brandon T., Allegheny Health Network, Pittsburgh, Pennsylvania, United States
Introduction

Hypothyroidism often manifests with a broad range of muscular symptoms: cramping, generalized weakness, and diffuse myalgias. Rhabdomyolysis is a rare manifestation of severe hypothyroidism resulting in profound acute tubular necrosis via myoglobin induced renal vasoconstriction, proximal tubule necrosis, and distal tubular obstruction. We present a case of acute tubular necrosis caused by rhabdomyolysis secondary to severe hypothyroidism.

Case Description

A 62-year-old female with past medical history of coronary artery disease, type II diabetes mellitus and hypothyroidism presented with fatigue, shortness of breath, fifteen pound weight gain and decreased appetite for a month. She reported myalgias and non-compliance with oral synthroid for seven months. Vital signs revealed normothermia without bradycardia. Physical exam was unremarkable. Laboratory work revealed elevated creatinine kinase (CK) 59,952 U/L, creatinine 6.37 mg/dL (baseline 0.8-1), very low free T4 <0.1 and very high TSH >1000. Urinalysis was positive for blood with minimal red blood cells, and urine sediment revealed granular casts. Treatment with intravenous fluids and synthroid significantly improved the TSH (75.9 mIU/L) and CK (10,791 U/L) on admission day ten. Renal function slowly improved over the hospitalization course with serum creatinine trend 6.37 mg/dL to 3.8 mg/dL on discharge with concurrent non-oliguric urine output. She was discharged home with oral thyroid hormone replacement therapy. She demonstrated complete renal recovery on outpatient follow up with serum creatinine 0.72 mg/dL, normal CK levels 31 U/L and thyroid function panel (TSH 0.97, free T4 1.5).

Discussion

The precise mechanism of hypothyroidism-induced rhabdomyolysis is unclear, however, it is thought to be related to impaired glycogenolysis or mitochondrial oxidation. This case is unique as there are no previously reported instances of patient sustaining such severe hypothyroidism-induced rhabdomyolysis (serum CK 400x upper limit of normal), and ATN in the absence of underlying chronic kidney disease. Therefore, prompt diagnosis, identification of causative factor, and timely treatment are crucial to prevent long-lasting renal injury in this disease. It also emphasizes medication compliance, patient education, and considering hypothyroidism in the differential diagnosis of rhabdomyolysis for improved patient outcomes.