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.
A 55-year-old Caucasian woman on peritoneal dialysis for the last three years due to lupus nephritis was seen in the dialysis clinic for a routine follow-up. Her medical problems included hypertension, secondary hyperparathyroidism, and documented osteoporosis on DEXA scan (Dual energy X-ray absorptiometry) with left femoral neck BMD at 0.637 g/cm2; 2.9 standard deviation below peak BMD. Her medications included Amlodipine 5mg, Cinacalcet 60 mg, and Epoetin weekly injections.\nShe complained of fatigue, muscle cramps, and paresthesias of the hands and feet for the past week. Vital signs were stable. Physical exam was unremarkable with negative Chvostek's and Trousseau's signs. Laboratory work-up showed profound hypocalcemia with a total calcium level of 6.4 mg/dL with corrected calcium level of 6.9mg/dL (serum albumin level of 3.4 g/dL) and markedly increased serum intact PTH level (iPTH) of 2601 pg/mL (). Serum phosphate and serum alkaline phosphatase level was within normal reference range at 3.1 mg/dl and 84 U/L, respectively. Upon history taking, she was found to have received a new medication, denosumab 60mg subcutaneously, prescribed by her rheumatologist 10 days prior to the current presentation.\nBefore the administration of denosumab, the patient had normal serum values of calcium (9.5 mg/dL), phosphorus (3.8 mg/dL), alkaline phosphatases (96 U/L), and 25 vitamin D with slightly elevated iPTH level at 442 pg/mL. The patient was supplemented with 3,000 mg/dL of oral calcium along with oral Calcitriol 0.5mcg daily and Cinacalcet was held. The peritoneal dialysis solution was also changed from low calcium to regular calcium. All these measures resolved her symptoms with serum calcium normalizing (corrected calcium, 8.7 mg/dL) 5 days later whereas iPTH took almost 4 weeks to come back to baseline level (). Subsequently, she was managed as an out-patient with close monitoring of calcium homeostasis.