Table 1

Inclusion and exclusion criteria for plasma exchange studies

Study Id

Inclusion criteria

Exclusion criteria

Cole 1992

RPGN of undefined aetiology (idiopathic or post infectious disease) with specific pathologic criteria.

Cellular crescents in < 50% non-obsolescent glomeruli.

Evidence of serious infection or active ulcer disease.

Adults (16-75 y), normal sized kidneys SCr > 170 μmol/L and/or increasing by 44 μmoles/l per wk.

No evidence of systemic disease or anti-glomerular basement membrane antibody-induced disease.

Renal biopsy within 5 days of trial entry

Jayne 2007

Biopsy-proven ANCA-associated necrotizing GN with acute kidney failure (SCr > 500 μmol/L)

Age <18 or > 80 years.

Inadequate contraception; pregnancy; previous malignancy; hepatitis B antigenaemia or hepatitis C antibody or HIV infection; other multi-system autoimmune disease; circulating anti-GBM antibody or linear staining of GBM on histology; life-threatening non-renal manifestations of vasculitis.

Dialysis for > 2 weeks before entry; creatinine >200 uM more than 1 year before entry. > 2 weeks treatment with CPA or AZA; > 500 mg of IV methylprednisolone; plasma exchange within the preceding year; >3 months treatment with oral prednisolone; allergy to study medications.

Glockner 1988

RPGN with >70% crescents on renal biopsy.

CrCl < 50 ml/min.

Urine output > 200 ml/24 h.

Anti-GBM disease, life threatening conditions, contraindications to immunosuppression, previous treatment with AZA or CPA for >14 days.

Mauri 1985

Histologically proven crescentic GN and rapidly progressive renal impairment.

Less than 60% glomerular involvement, primary glomerulopathies, transplanted kidneys, SLE, HSP.

Pusey 1991

Focal necrotizing GN with crescents (Wegener's granulomatosis, systemic vasculitis, polyarteritis, idiopathic RPGN)

Anti-GBM disease, SLE, Henoch-Schonlein Purpura, chronic GN Previously treated with IV MP, oral CPA or PE

Rifle 1980

New onset RPGN with > 50% glomerular crescents.

Goodpasture's syndrome; IgA nephropathies; SLE; systemic disease.

Walters et al. BMC Nephrology 2010 11:12   doi:10.1186/1471-2369-11-12

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