Fixation is to glomerular basement membrane, Bowmans capsule, and tubular basement membranes (arrows) (fluorescein isothiocyanate-conjugated rabbit anti-human IgG, 250). After surgery, hemodialysis was started and repeated three times a week, while the steroid dosage was gradually lowered. membrane.1, 3C5, 8, 12C25 In patients, many of whom were diagnosed on clinical grounds only, chronic systemic steroid therapy, other immunosuppressive agents, and hemodialysis have been inconsistent or valueless in controlling either these renal or pulmonary symptoms.11, 16C22 This paper reports three patients with anti-GBM antibody mediated glomerulonephritis and pulmonary hemorrhage treated initially with splenectomy and bilateral nephrectomy 7 to 37 months ago. After circulating anti-GBM antibodies could no longer be detected, each patient received a renal homograft. Methods General Care The surgical procedures and the general principles of postoperative care have been described elsewhere.23 Immunosuppression with azathioprine, Bimatoprost (Lumigan) prednisone, and equine antilymphocyte globulin (ALG)24 was begun two to four days before transplantation. The subsequent timing and dosage of the individual brokers are shown in Fig 1 to ?to3.3. The recipients ages, the timing of surgical interventions, and the source and match of kidney homografts are shown Bimatoprost (Lumigan) in the Table. Open in a separate window Fig 1 Course of 30-year-old male patient (case 1). Open in a separate window Fig 3 Course of 35-year-old male patient (case 3) Table Case Material
Date of onset10/1/679/13/685/29/70Age of patient, yr302935Date of splenectomy and nephrectomies1/24/682/4/698/19/70Date of transplantation4/29/687/3/691/28/71Kidney donorBrotherBrotherSisterTerasaki matchAADTime of posttransplantation, mo3420 Open in a separate window Detection of Renal Bound and Circulating Anti-GBM Antibodies Snap frozen renal nephrectomized and biopsied specimens were examined for glomerular-bound human immunoglobulins (IgG, IgA, and IgM), complement (C3), fibrin, albumin, and equine immunoglobulin by Rabbit Polyclonal to ALS2CR13 direct immunofluorescence.25 Anti-GBM antibodies eluted from this renal tissue with hypotonic citrate buffer (pH 3.2) were detected by indirect immunofluorescence on normal human kidney sections.7,8 Circulating anti-GBM antibodies were sought by indirect immunofluorescence using normal human kidney sections.26 Preformed cytotoxic antibodies against donor lymphocytes were ruled out in all three cases by the direct cross-match method of Terasaki.27 Report of Cases Case 1 A 30-year-old white man was admitted to the Denver Veterans Administration Hospital with a two-day history of hematuria. Within one week he developed hemoptysis, fluffy infiltrates throughout both lung fields, and oliguria (250 ml/24 hr). A closed renal biopsy revealed necrotizing glomerulitis. Prednisolone (120 mg/day) did not halt progressive renal failure (Fig 1), necessitating hemodialysis; however, the lung fields cleared rapidly. He was treated with variable daily doses (usually 2 mg/kg/day) of mercaptopurine between the 11th and 30th days following admission. In January 1968, 115 days after the onset of symptoms, elective splenectomy and bilateral nephrectomy were performed. A severe, crescent-forming, subacute glomerulonephritis was present histologically (Fig 4). Anti-GBM antibodies were present in the kidneys and in Bimatoprost (Lumigan) the circulation. Renal homotransplantation followed after an additional 95 days when circulating anti-GBM antibodies had disappeared. There were no rejection episodes, and the normally functioning homograft was biopsied 34 months posttransplantation. No glomerular abnormalities were present by light microscopy (Fig 5). Open in a separate window Fig 4 Crescent forming subacute glomerulonephritis found in native kidneys of patients in case 1 (lett), case 2 (center), and case 3 (right) (PAS, 340). Open in a separate window Fig 5 Normal histologic appearance of representative glomeruli from Bimatoprost (Lumigan) renal homograft biopsies of case 1 (left) 34 months posttransplantation and case 2 (right) 20 months posttransplantation (PAS, 340). Case 2 A 29-year-old white man had recurrent bronchopneumonia in September and October of 1968, associated with dyspnea and hemoptysis. On Jan 8, 1969, he was hospitalized in another city for these pulmonary symptoms and gross hematuria. Laboratory studies disclosed the following values: hematocrit reading, 20 %; blood urea nitrogen (BUN), 60 mg/100 ml; and antistreptolysin titer, 250 Todd units/100 ml (slightly elevated). Blood pressure Bimatoprost (Lumigan) was 160/80 mm Hg..
