Case Presentation: A 58-year-old woman presented with 10 hours of left lower extremity pain and decreased urine output. The patient had a history of total thyroidectomy decades prior and had been prescribed levothyroxine. It was stopped two months prior to admission for low TSH.She had 2+ edema bilaterally.Labs returned with a creatinine of 6.8 mg/dL, potassium of 6.4 mmol/L, CK of 42,000 U/L, TSH of 361 uIU/mL, and Free T4 of .29 ng/dL. FENA was 2.4% and FEUrea was 51%. The patient failed to produce urine and required initiation of hemodialysis. ANA and ENA panels were negative. Myositis panel including Mi-2, Ku, SRP, PL-7, PL-12, EJ, OJ, and HmgCoA reductase antibody were negative. MRI of lower extremities revealed extensive myositis involving of bilateral quadriceps muscles. Pathology report from right vastus lateralis biopsy noted no evidence of myositis. Due to bilateral distribution of myositis seen on imaging as well as the extent of CK elevation which peaked at 55,000 U/L, it was thought that her myopathy was secondary to a metabolic cause, most likely hypothyroidism.She was discharged to her nursing home on HD and levothyroxine. Her renal function did not recover. She was readmitted 5 weeks after discharge for dry gangrene. Her stay was complicated by thrombocytopenia, hypotension, and UTI. She was transferred to the ICU and started on IV antibiotics. As she was a poor surgical candidate she was made DNR/DNI and discharged to inpatient hospice. She died three days later.
Discussion: Hypothyroidism is a rare but well-established cause of myopathy with case reports occasionally demonstrating CK levels in excess of 20,000 U/L. In any patient presenting with extensive muscle damage, avoiding or treating acute kidney injury from myoglobin toxicity is among the clinician’s foremost concerns. Given this, it is not surprising that a review of literature provides several case reports of patients presenting with the triad of hypothyroidism, myopathy, and kidney failure. While conventional wisdom holds rhabdomyolysis as a well-known cause of intrinsic kidney injury, kidney failure in hypothyroid myopathy may be mediated not only by myoglobin toxicity, but also by the metabolic effects of hypothyroidism itself. The positive association between GFR and thyroid activity has been reported as far back as 1957, with Kuhlback et al finding an increase in serum creatinine among hypothyroid patients and a decrease in creatinine in hyperthyroid patients. It has been proposed that thyroid activity increases GFR through a variety of mechanisms. Thyroid hormone’s chronotropic and ionotropic effects increase cardiac output and thereby also renal blood flow. Additionally, thyroid hormone increases GFR by activating RAAS. Retrospective studies have confirmed a clinical association between hypothyroid state and decreased GFR as well as hyperthyroidism and increased GFR.
Conclusions: This case illustrates thyroid hormone’s complex interplay with renal function and how the state of hypothyroidism itself may contribute to acute kidney injury.