A 59-year-old postmenopausal woman with a past medical history of Billroth II gastric bypass surgery 15 years before for bariatric purposes, Barrett esophagus, pericarditis secondary to suspected rheumatologic disease status treated with a pericardial window 3 years before, rheumatoid arthritis with negative rheumatoid factor, paroxysmal atrial fibrillation, amiodarone-induced hypothyroidism, and osteoporosis treated with denosumab 3 months before was referred to the emergency department by her endocrinologist after outpatient labs revealed profound hypocalcemia, hypophosphatemia, and hypomagnesemia. The patient had recently returned from vacation, where she experienced 2-3 episodes of diarrhea. She reported compliance to her medications, which included 50,000 IU ergocalciferol daily and 630 mg calcium citrate 2-3 times daily, apart from taking a decreased dose of calcium for the last 4 days of her vacation since she was running low on pills. She noted fatigue and intermittent tingling in her hands, feet, and perioral region for 2-3 days prior to admission. She denied weight loss, fever, muscle cramping, seizures, loss of consciousness, or lightheadedness.\nOn presentation, the patient was afebrile with a temperature of 98.2ºF, blood pressure of 136/74 mmHg, heart rate of 71 beats/min, and respiratory rate of 15 breaths/min. Her oxygen saturation was 100% on room air. Physical examination revealed a well-appearing woman with a body mass index (BMI) of 30 kg/m2 in no acute distress. Neck was supple with no thyromegaly. There were no abnormalities on cardiac or pulmonary exam. Abdomen was soft, nontender, and nondistended with normal bowel sounds. Patient had a positive Chvostek's sign. No muscle twitches or spasms were appreciated. Strength, sensation, reflexes, and cranial nerves were intact. The patient had no signs of confusion or psychosis.\nBlood tests from the emergency department revealed a calcium of 5.8 mg/dL, phosphorus of <1 mg/dL, and magnesium of 1.7 mg/dL. Albumin was 3.8 g/dL, so the corrected calcium was 6.0 mg/dL. Ionized calcium was 0.8 mg/dL. Parathyroid hormone was 136 ng/L. 25-Hydroxy vitamin D was normal at 46 ng/mL, and 1-25-hydroxy vitamin D was normal at 30 pg/mL. Urinalysis was within normal limits, and urine calcium was <2 mg/dL. Creatinine was 0.61 mg/dL, and blood urea nitrogen was 11 mg/dL. TSH was normal at 0.78 μU/mL. An electrocardiogram performed in the emergency department showed normal sinus rhythm with a corrected QT interval of 493 ms.\nIn the emergency department, the patient was given 2 g of IV magnesium sulfate, 30 mmol of IV sodium phosphate, and 1 g of IV calcium gluconate. During her 4-day hospital stay, the patient continued to receive IV calcium, as well as oral calcitriol, phosphate, and magnesium. When she was able to consistently maintain serum calcium of at least 8.0 mg/dL on oral calcium citrate supplementation, she was discharged with a calcium level of 8.0 mg/dL, magnesium of 1.9 mg/dL, and phosphorus of 2.3 mg/dL. She was instructed to take calcium citrate of 1260 mg 4 times daily, calcitriol of 0.25 mcg 2 times daily, phosphorus of 250 mg 3 times daily, and magnesium oxide of 400 mg 2 times daily and to be followed up closely with her endocrinologist. Since discharge, the patient has been able to maintain adequate calcium levels on a low dose of calcium supplementation, and she is interested in considering further doses of denosumab.
A 17-year-old 6-week-pregnant female was admitted for nausea and vomiting for a suspected morning sickness. At admission patient was found to have a mild fever of 99 F, hemoglobin of 6.5 mg/dL, and serum creatinine at 6.47 mg/dL. Baseline creatinine six months earlier was 0.6 mg/dL. A thrombotic thrombocytopenic purpura was suspected despite normal platelets and hence she was admitted to the hospital for further workup. Vital signs at admission were temperature of 99 F, heart rate of 90–100 beats per minute, respiratory rate of 14 cycles per minute, and blood pressure of 120–130/80 s. Physical exam was consistent with a normal female who was moderately built without any evidence of fluid overload like raised jugular venous distension and facial or leg edema. Heart and lung exam were within normal limits. Patient's neurological exam was intact. Laboratory findings were as follows: hemoglobin 6.51 mg/dL, white blood cell count 10.3 k/mm3, platelets 384 k/mm3, sodium 136 mEq/L, potassium 4.4 mEq/L, chloride 107 mEq/L, bicarbonate 21 mEq/L, blood urea nitrogen 26 mg/dL, and creatinine 6.47 mg/dL. Iron studies showed iron deficiency anemia with iron of 25 mcg/dL, total iron binding capacity of 185 mcg/dL, iron saturation of 14%, and transferrin of 132 mg/dL. Urine analysis at admission showed urine pH of 6.5, specific gravity of 1.009, urine protein of 2+, and urine blood of 3+ with too numerous RBCs to count; urine glucose, ketones, bilirubin, and leukocyte esterase were all negative. Other tests that were ordered were antiglomerular basement membrane antibodies which were high at 156 units. Complement C3 and C4 levels were high at 195 and 57, respectively. Antineutrophil antibody, antineutrophil cytoplasmic antibody, antiproteinase 3, anti-Smith, and ds DNA were negative. Other miscellaneous lab tests like HIV antibody, hepatitis A IgM antibody, hepatitis B surface antigen, hepatitis B core IgM antibody, hepatitis C antibody, and antistreptolysin O Ab were all negative.\nOn the second day of hospitalization the patient underwent a kidney biopsy for a suspected anti-GBM disease. The preliminary biopsy results based on the hematoxylin and eosin stains showed acute necrotizing and crescentic glomerulonephritis. Final pathology results showed acute crescentic glomerulonephritis with no globally obsolescent glomeruli, moderate interstitial inflammation, and mild fibrosis. The final images of the pathology slides are shown in Figures and .\nPatient was given 2 units of PRBC after admission with a posttransfusion Hb at 8.9 mg/dL. Peripheral smear did not show any schistocytes and hence the diagnosis of TTP was ruled out. All the labs and pathology suggested acute anti-GBM disease. On hospital day 3 plasmapheresis and high dose methylprednisolone at 1 gm/day were begun. See for creatinine trend. Creatinine peaked to 7.48 on day 5 and the patient was slowly becoming oliguric, showing sign of fluid overload with pedal edema and lung crackles on physical exam and hence was initiated on intermittent hemodialysis on day 5 of hospitalization. Patient received a total of 3 doses of methylprednisolone at 1 gm/day and then was started on prednisone at 60 mg/day from day 4.\nTo prevent further renal injury the option of adding cyclophosphamide was discussed but was not done due to possible fetal adverse outcomes. On day 17 of hospitalization the patient had a spontaneous abortion. After abortion cyclophosphamide was not started due to patient's request and hence she was managed with plasmapheresis and high dose prednisone. The plasmapheresis sessions were started on day 3 and continued daily until discharge (day 25). Traditional plasmapheresis with albumin replacement and sometimes 70% albumin with 30% normal saline replacement that lasted for 3 hours every day was the technique used. She was never started on cyclophosphamide and slowly became hemodialysis independent in about 2 months from discharge. At about 6 months from discharge the patient lost to follow up. It was deemed that the acute anti-GBM flare-up was pregnancy related.