We report a 77-year-old Caucasian female who had presented to nephrology clinic with a history of multiple sclerosis in remission who was noted to have progressive weakness for 2 months prior to presentation. Suspicion for a multiple sclerosis flare was low since her electrolytes were grossly abnormal with a serum calcium of 13.7 mg/dL and a serum creatinine of 2 mg/dL on June 23, 2017, increased from baseline of 8 - 9 mg/dL (calcium) and 0.9 - 1.1 mg/dL (creatinine). Ionized calcium was measured at 1.54 mmol/L (reference range 1.09 - 1.29 mmol/L), confirming the hypercalcemia noted on chemistry. Patient had initially been taking cholecalciferol 2,000 units PO daily for osteoporosis prophylaxis which were stopped, but this failed to improve the serum calcium. Parathyroid hormone (PTH) was appropriately suppressed at low normal 18 - 21 pg/mL (reference range 11 - 51 pg/mL), PTH-related peptide was in range at 17 pg/mL (reference range 14 - 27 pg/mL) which was not consistent with hypercalcemia of malignancy. The patient had normal sodium and alkaline phosphatase values. Urinalysis showed only 1+ proteinuria and was otherwise normal, and the kidney ultrasound demonstrated normal kidney structure. 25-hydroxy vitamin D level was 28 - 37 ng/mL (reference range: 20 - 50 ng/mL), but 1,25-dihydroxy vitamin D levels remained elevated despite stopping any supplements and remained elevated for nearly 2 months. 1,25-dihydroxy vitamin D peak level was 158 pg/mL (reference range: 19.9 - 79.3 pg/mL) and remained elevated between 100 and 113 pg/mL despite stopping vitamin D supplements. Urine protein electrophoresis and serum electrophoresis were negative or an M-spike, immunofixation was only positive in serum with IgG-kappa monoclonal being found. kappa- and lambda-light chains were only slightly skewed towards IgG-kappa > IgG-lambda with a ratio of 2.32, ruling out monoclonal gammopathy as the etiology for the hypercalcemia. 
The patient's hypercalcemia continued to cause acute kidney injury, her calcium reached 12.6 mg/dL, she was hospitalized where she was given IV fluids, furosemide, and pamidronate. A high resolution CT scan did not show any lymphadenopathy or pulmonary pathology (Figure 1), and angiotensin-converting enzyme levels were elevated at 100 U/L and 102 U/L for 2 draws. After the aforementioned treatment, her serum calcium decreased to 10.5 mg/dL. 
When her serum calcium increased to 11.8 mg/dL, she was given denosumab 120 mg formulation in the interim leading to the return of serum calcium to 10.5 mg/dL. Since infectious causes of granulomatous diseases, such as tuberculosis and fungal infections, were in the differential diagnosis corticosteroids were not given empirically. While the high level of angiotensin-converting enzyme suggested possible sarcoidosis, we considered the low specificity of the test to demand more definitive tissue diagnosis could be obtained. Thus, corticosteroids were deferred until definite diagnosis, and denosumab was prescribed in the interim to control hypercalcemia. 
See Figure 2 for graphs of serum calcium, PTH, 25-hydroxy vitamin D, 1,25-dihydroxy vitamin D, angiotensin-converting enzyme level, and serum creatinine levels. Mycobacterial serologies, coccidiomycosis, and other fungal serologies were negative as well. 
It was during this time that granulomatous disease, specifically sarcoidosis was suspected. She underwent PET scan with findings of upper lobe predominant peri-bronchial wall thickening, diffuse lymphadenopathy and flourodeoxyglucose (FDG) uptake throughout pulmonary parenchyma. This was suggestive of a granulomatous process such as sarcoidosis. No other focus of FDG uptake in a pattern that suggests malignancy was found, and no splenic involvement was seen. See Figure 1 for PET scan image and findings. 
When the patient's creatinine increased to 2.58 mg/dL with a serum calcium of 11 mg/dL, the patient was admitted for definitive diagnostic procedures. Bone marrow biopsy and a transbronchial lymph node biopsy were obtained. The patient's serum calcium and serum creatinine normalized with hydration and subcutaneous calcitonin injection. Biopsy results showed diffuse non-necrotizing/non-caseating granulomata in lung and bone marrow confirming diagnosis of systemic sarcoidosis. Cultures from lung biopsy were negative for mycobacteria, fungal elements, or bacteria. The sarcoidosis staging was rated at stage 0 according to lung imaging, but with a high enough burden of disease to cause significant hypercalcemia. Please see Figure 3 for details of biopsy findings and bone marrow biopsy results. The patient started 20 mg of prednisone after diagnosis with improvement of hypercalcemia down to serum calcium of 10.2 mg/dL. She is receiving 3 times weekly hydration with IV normal saline to help prevent dehydration which helped decrease serum creatinine to 1.58 mg/dL. The patient was not on TNFi (tumor necrosis factor) to suggest secondary sarcoidosis. Her multiple sclerosis was stable as well. She was started on plaquenil for maintenance treatment of the diagnosed sarcoidosis.