Chronic graft-versus-host disease (cGVHD) is a leading cause of non-relapse mortality in allogeneic hematopoietic cell transplant (HCT) recipients. While the current standard of care is proactive in detecting cGVHD in the lungs, liver, and skin, cGVHD involving kidneys is an underrecognized and likely underdiagnosed cause of post-HCT renal dysfunction. Nephrotic syndrome (NS) is a very rare complication of HCT that is postulated to be a glomerular manifestation of cGVHD. Herein, we report 2 cases of post-HCT minimal change disease likely secondary to cGVHD. In both cases, the onset of NS coincided with tapering of calcineurin inhibitors, and 1 patient had previously been diagnosed with cGVHD of the lungs. One patient was treated with corticosteroids alone and the other with a corticosteroids and tacrolimus. Complete, sustained remission was achieved in both cases. Our cases illustrate the implications of the association between cGVHD and post-HCT NS for patient care, including the importance of obtaining a renal biopsy to establish an accurate histopathological diagnosis and guide-appropriate treatment.

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Background: Myxedema coma (MC) represents severe decompensated hypothyroidism and is associated with mortality rates up to 50%. It is precipitated by an acute event which disrupts compensatory mechanisms present in severe hypothyroidism. Treatment includes IV levothyroxine (LT4) with consideration of liothyronine (LT3) therapy and management of any underlying stressor. Here we present a case of MC and adrenal crisis due to pituitary dysfunction successfully treated with IV LT4 and LT3. Case: A 55-year-old female with no pertinent medical history presented with two weeks of shortness of breath, anorexia, fatigue, and unexplained falls. Her initial vital signs were notable for a blood pressure of 86/60, temperature of 36.3 °C, heart rate of 59, SpO2 of 86 on room air, and respiratory rate of 21. Exam was notable for altered mentation, respiratory distress, decreased bowel sounds, and edematous facies. Initial serum studies were notable for sodium of 133 mmol/L (135-145 mmol/L), blood glucose of 50 mg/dL (74-99 mg/dL), TSH of 2.1 mIU/L (0.45-4.50 mIU/L), and blood gas showed pH of 7.27 and PaCO2 of 84.7 mmHg. She was intubated, started on vasopressors, and IV hydrocortisone 100 mg was administered. Her pretreatment serum cortisol was unmeasurable (below 0.5 mcg/dL) and ACTH resulted at 2.0 pg/mL (7-63 pg/mL). Despite hydrocortisone 50 mg q8h, her vitals worsened with HR to 40 bpm and temperature to 34.4 °C. Given concerns for MC, free and total T4 tests were obtained and both were undetectable (below 0.4 ng/dL and 4.0 ug/dL, respectively), so 300 mcg IV LT4 was administered. The next day, the patient’s vasopressor requirement increased, so 5 mcg IV LT3 q8h was added and IV LT4 was maintained at 100 mcg/day. Total T4 and T3 were measured daily and increased into the reference range over the course of 8 days and 2 days, respectively. LT3 was discontinued after 8 days and LT4 was converted to oral regimen of 125 mcg LT4 (weight expected 115 mcg) on day 14 after extubation; her hydrocortisone was tapered to a daily total of 30 mg PO. An MRI of pituitary showed an empty sella with a thin rim of normal appearing tissue without other lesions. The patient later denied any history of post-partum hemorrhage, idiopathic intracranial hypertension, pituitary surgery, radiation, or trauma. She is currently doing well on LT4 and hydrocortisone replacement. Conclusion: This case highlights the successful use of combined LT4 and LT3 in the treatment of MC with concomitant adrenal crisis. LT3 therapy may have been particularly beneficial in this case as conversion of T4 to T3 may be limited in setting of severe illness and high-dose glucocorticoid administration. Limited observational literature suggests that LT3 use can have clinical benefit, although excessive LT3 dosing may be associated with increased mortality. Further research is required to elucidate the benefits of empiric LT3 use in MC with concurrent adrenal insufficiency.