Plasmapheresis in treatment of acute oligoanuria in crescentic glomerulonephritis.
Plasmapheresis therapy can provide an approach in the treatment of crescentic glomerulonephritis by mechanically removing nephritogenic factors from the circulation, both antiglomerular basement membrane antibodies and circulating immune complexes as well as antineutrophil cytoplasmic antibodies (ANCAs). We present our experience with plasmapheresis treatment in patients with acute oligoanuria caused by crescentic glomerulonephritis. We used membrane plasmapheresis to treat 11 patients with crescentic glomerulonephritis with more than 80% crescent formation on biopsy and with acute onset of the disease and acute oligoanuria. The immune complex form of the disease was documented in 7, the antiglomerular basement membrane antibodies mediated (anti-GBM) form in 2, the ANCA-associated form in 1 case, and the recurrent anti-GBM form in 1 patient. Plasmapheresis was performed 2-3 times weekly using Bellco BL 500 and Gambro 2000 PF plasma filters. The total number of plasma exchanges (2,000-2,200 ml each) for each patient was 5-9. The treatment was associated with steroids and cyclophosphamide. The improvement of renal function with the start of diuresis and significant decrease of creatinine from the range of 786-1,301 microM at the start of the treatment was noted in 5 of the 11 patients. The duration of remission without hemodialysis was 6-12 months. Treatment with plasmapheresis in cases with recurrent anuria was without benefit. We can conclude that plasmapheresis can delay end-stage renal failure in cases with acute onset of crescentic glomerulonephritis.
Grcevska
L
L
Department of Nephrology, University Clinical Center, Skopje, Republic of Macedonia.
Polenaković
M
M
Stojkovski
L
L
Polenaković
H
H
D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000097:blood; D000936:Antigen-Antibody Complex / Q000097:blood; D001002:Anuria / Q000209:etiology / Q000628:therapy*; D001323:Autoantibodies / Q000097:blood; D001485:Basement Membrane / Q000276:immunology; D003404:Creatinine / Q000097:blood; D003520:Cyclophosphamide / Q000627:therapeutic use; D004231:Diuresis; D004847:Epithelial Cells / Q000473:pathology; D005260:Female; D005921:Glomerulonephritis / Q000097:blood / Q000150:complications / Q000628:therapy*; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007668:Kidney / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000517:prevention & control; D007678:Kidney Glomerulus / Q000276:immunology; D008297:Male; D008567:Membranes, Artificial; D008775:Methylprednisolone / Q000627:therapeutic use; D010951:Plasma Exchange; D010956:Plasmapheresis / Q000295:instrumentation / Q000379:methods; D012074:Remission Induction; D006435:Renal Dialysis
D019268:Antibodies, Antineutrophil Cytoplasmic; D000936:Antigen-Antibody Complex; D001323:Autoantibodies; D005938:Glucocorticoids; D007166:Immunosuppressive Agents; D008567:Membranes, Artificial; D003520:Cyclophosphamide; D003404:Creatinine; D008775:Methylprednisolone