OBJECTIVE: Nephritis has been rarely associated with methimazole, primarily in the development of nephrotic syndrome. We describe a case of acute kidney injury without evidence of nephrotic syndrome following methimazole initiation. METHODS: We present the relevant history, laboratory data, and nuclear medicine data and review relevant documentation from the literature. RESULTS: A 72-year-old male recently diagnosed with new-onset atrial fibrillation was found to have suppressed thyroid-stimulating hormone (TSH) levels; elevated free T3, T4, and thyroid-stimulating immunoglobulin (TSI) levels; and a nonnodular thyroid gland with normal iodine uptake. He was diagnosed with Graves' disease and treated with propylthiouracil (PTU) for 5 years. When his poor compliance with PTU was impeding his antithyroid treatment, he was converted to methimazole. Within 1 month following methimazole initiation, his serum creatinine (SCr) had risen to 1.6× baseline in the absence of other contributing nephrotoxins. SCr returned to baseline within 2 weeks of methimazole discontinuation, and the patient was subsequently managed on PTU. CONCLUSION: Acute kidney injury with or without the presence of nephrotic syndrome may occur during treatment with methimazole. Renal function should be closely monitored after the initiation of methimazole to prevent progressive renal dysfunction.
OBJECTIVE: Nephritis has been rarely associated with methimazole, primarily in the development of nephrotic syndrome. We describe a case of acute kidney injury without evidence of nephrotic syndrome following methimazole initiation. METHODS: We present the relevant history, laboratory data, and nuclear medicine data and review relevant documentation from the literature. RESULTS: A 72-year-old male recently diagnosed with new-onset atrial fibrillation was found to have suppressed thyroid-stimulating hormone (TSH) levels; elevated free T3, T4, and thyroid-stimulating immunoglobulin (TSI) levels; and a nonnodular thyroid gland with normal iodine uptake. He was diagnosed with Graves' disease and treated with propylthiouracil (PTU) for 5 years. When his poor compliance with PTU was impeding his antithyroid treatment, he was converted to methimazole. Within 1 month following methimazole initiation, his serum creatinine (SCr) had risen to 1.6× baseline in the absence of other contributing nephrotoxins. SCr returned to baseline within 2 weeks of methimazole discontinuation, and the patient was subsequently managed on PTU. CONCLUSION: Acute kidney injury with or without the presence of nephrotic syndrome may occur during treatment with methimazole. Renal function should be closely monitored after the initiation of methimazole to prevent progressive renal dysfunction.