Minimal Change Disease (MCD) is identified via renal biopsy as the etiology of nephrotic syndrome in a minority of adult cases; however, a significant proportion of these occurrences are accompanied by acute kidney injury (AKI). Risk factors for AKI in MCD include increased age, male sex, hypertension, and marked proteinuria and hypoalbuminemia. The etiology of AKI appears to be tubular injury as demonstrated with biomarkers, and although it is usually reversible with steroid therapy, resistance and relapses can occur and may require the use of second-line agents. We present a case of an adult patient with acute onset of biopsyproven MCD and AKI demonstrating a partial response to corticosteroids and aggressive diuresis and later relapsing and requiring further immunosuppression with tacrolimus. Ultimately, further studies are required to determine the optimal treatment regimen for MCD to ensure remission and avoid relapse.

We report a case of a middle-aged female who presented with altered mental status, hypotension, and hypoglycemia and was diagnosed with secondary adrenal insufficiency. She was also found to have elevated troponin I on initial evaluation with diffuse T wave inversions on electrocardiogram. Transthoracic echocardiogram revealed ejection fraction of 38% with apical akinesia. Subsequent left heart catheterization revealed clean coronary arteries. She was diagnosed with typical Takotsubo cardiomyopathy secondary to adrenal insufficiency. She was managed with IV hydrocortisone with resolution of symptoms. This article adds to the select few cases in the literature of the association of Takotsubo cardiomyopathy resulting from secondary adrenal insufficiency.

Langerhans cell histiocytosis (LCH) is a rare malignancy most commonly characterized by histiocytic infiltration of bone. LCH lesions in the skull place the adjacent central nervous system (CNS) at risk for involvement, which can manifest as central diabetes insipidus (CDI) when there is infiltration of the hypothalamic-pituitary axis. We present a case of a 39-yearold female who presented with polyuria and polydipsia for 1 year and left-sided hearing loss, gait instability, and nystagmus for 5 days. She was found on laboratory evaluation to have CDI and underwent left cortical mastoidectomy for a destructive peripherally enhancing mastoid lesion seen on MRI brain. Pathology revealed CD1a and S100+ LCH and the patient was subsequently discharged to begin outpatient chemotherapy with vinblastine and prednisone. The patient's CDI was diagnostic of CNS involvement, making her LCH multisystem through the infiltration of both the skull and hypothalamic-pituitary structures. As CDI can be seen in up to 25% of single-system LDH, and up to 50% of multisystem cases, radiologic studies to evaluate for osteolytic skull lesions must be considered as part of the evaluation for LCH when CDI has been diagnosed.