Al-Harbi et al5described a 30-year-old female with rapidly progressive glomerulonephritis due to anti-GBM disease who needed dialysis during her pregnancy until delivery. patient was transferred to University of Oklahoma Medical Center for further evaluation of her acute renal failure. On transfer, temperature was 36. 4C, heart rate was 89 is better than per minute, respiratory rate was 16 cycles per minute, and blood pressure was 147/61 mm Hg. Physical exam exposed obesity (body mass index = 43 kg/m2) but was otherwise unremarkable. Specifically there was no evidence of fluid overload. Laboratory findings were as follows: hemoglobin 6. 51 g/dL, white blood cell count number 10 300/mm3, platelet count number 384 000/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. Serum iron Resiquimod studies showed an iron of 25 g/dL, total iron binding capacity of 185 g/dL, iron saturation of 14%, and ferritin of 170 ng/mL. Urine analysis at admission showed pH of 6. 5, specific gravity 1 . 009, 2+ Resiquimod protein, 3+ blood, and too several red blood cells (RBCs) to count number. Urine glucose, ketones, bilirubin, and leukocyte esterase were all unfavorable. Urine sediment was examined by the Nephrology Consult Team and was remarkable intended for too several to count number RBCs and one RBC cast. Around the second day of hospitalization, the patient underwent a kidney biopsy in an effort to determine the etiology of her acute renal failure. Additional laboratory studies were also obtained including antiglomerular basement membrane (GBM) antibodies, enhance C3 and C4 levels, antineutrophil antibodies, antineutrophil cytoplasmic antibodies, antiproteinase 3, anti-Smith, anti-double-stranded DNA, HIV antibody, hepatitis A IgM antibody, hepatitis W surface antigen, hepatitis W core IgM antibody, hepatitis C antibody, and antistreptolysin O. These test were pending at the time of the biopsy and were all consequently reported because unremarkable except the anti-GBM antibody, which was elevated at 156 arbitrary units. Hematoxylin and eosinstained sections of the renal biopsy showed acute necrotizing and crescentic glomerulonephritis (Figure 1). There were no globally obsolescent glomeruli; however , there was moderate interstitial inflammation and moderate interstitial fibrosis (Figure 2). Approximately half of the glomeruli had crescents, and approximately a third of the glomeruli had foci of necrosis. Immunofluorescence showed linear staining of the GBM for IgG consistent with anti-GBM disease (Figure 3). == Figure Resiquimod 1 . == Hematoxylin and eosinstained section of the renal biopsy showing crescentic glomerulonephritis with moderate interstitial inflammation and mild fibrosis with no evidence of vasculitis. == Figure 2 . == Low power (approximately 100) hematoxylin and eosinstained section of the renal biopsy showing crescentic glomeruli. == Figure three or more. == Immunofluorescence showing linear staining from the GBM staining for IgG. Two models of packed red blood cells were administered with a posttransfusion hemoglobin of 8. 9 g/dL. On hospital day three or more, plasmapheresis MMP10 was initiated. In addition , the patient was given intravenous methylprednisolone 1000 mg daily intended for 3 days, followed by oral prednisone 60 mg daily. The serum creatinine rose to 7. 48 on day 5, and the patient developed oliguria, showing signs of fluid overload with pedal edema and lung crackles. Thus, hemodialysis was initiated. The addition of cyclophosphamide was discussed at size with the patient and her family. In addition , Maternal-Fetal Medicine was consulted and emphasized that the wellness of the mother must be a priority. The patient was reluctant to initiate cyclophosphamide, since.
Al-Harbi et al5described a 30-year-old female with rapidly progressive glomerulonephritis due to anti-GBM disease who needed dialysis during her pregnancy until delivery
