Refractory Postsurgical Hypothyroidism in Nephrotic Syndrome

Abstract

Abstract 62-year-old female with a history of thyroid cancer of unknown type s/p thyroidectomy 30 years prior to presentation, who had 2 months of worsening generalized edema and increasing need of dose escalation of her oral thyroid replacement by her PCP. Despite increasing her thyroxine dose multiple times and adding Armour thyroid based on increasing TSH and decreasing FT4 on outpatient labs, her edema continued to get worse. She presented to the Emergency Department. She takes no other medications. Symptoms include malaise, cold intolerance, weight gain, hair loss, bloating without constipation,“feeling foggy” and that her memory seemed a bit “off”, and she felt her mood was more “sensitive”, and she had atypical non-exertional chest discomfort. On exam she was was bradycardic to 56 and hypertensive to 175 systolic, had faint bibasilar crackles were present bilaterally, had significant pitting edema of the bilateral lower extremities, 3+ up to the level of her abdomen, as well as pitting edema of her bilateral upper extremities, and no periorbital edema was seen. Her neurologic exam was non-focal. Outpatient labs included TSH 178, free T4 0.35, albumin 1.2, and BNP level of 57. Her liver and kidney function tests were normal. Hospital labs included a normal CBC, chemistry with an albumin of 2.2 and normal range liver and kidney function. Thyroid function tests included a very high TSH level of 141, low free T4 level of 0.37, and a free T3 toward the lower end of normal. Lipid panel showed severe hypercholesterolemia. Urine studies showed microhematuria as well as the equivalent of proteinuria to the level of 10 grams per day. HIV was negative and complement levels were within normal limits. CXR, renal US, transvaginal US, and CT chest/abdomen/pelvis were performed to investigate the proteinuria and potential secondary causes of the proteinuria, all of which were unremarkable for acute or pertinent findings. Pathology results from a kidney biopsy showed membranous nephropathy. The patient initially received IV steroids and IV thyroxine as well as an albumin infusion. She was quickly transitioned to oral thyroxine due to her stability on presentation. She was given a statin and ACE inhibitor as well as IV Lasix. And she was discharged on thyroxine, with Armour thyroid being discontinued. She had severe hypothyroidism in a patient dependent on exogenous thyroid hormone which was exacerbated by severe proteinuria due to a new-onset nephrotic syndrome. Her hospital course uneventful. She responded well to intravenous diuretics. After her diagnosis of membranous nephropathy, Nephrology recommended continued conservative treatment due to her normal renal function and improving edema with outpatient follow up. She only received a single dose of IV thyroxine and remained stable after switching to oral thyroxine.