title: Clinicopathological features of membranoproliferative glomerulonephritis under a new classification.
abstract: BACKGROUND
  A recent classification of membranoproliferative glomerulonephritis (MPGN) utilizes the presence of immunoglobulin and complements to simplify diagnosis and point towards disease etiology. Here, we evaluate a historic cohort of patients with idiopathic MPGN using the new classification system and correlate it with clinical outcome.
  
  
  METHODS
  We identified 281 patients diagnosed with MPGN at Stanford from 2000 to 2012. Patients with hepatitis, systemic lupus erythematosis, lymphomas, and plasma cell dyscrasias were excluded. The clinicopathologic findings of the remaining 71 patients were further analyzed and differences between immunoglobulin dominant (IM) and complement dominant (CM) disease were evaluated.
  
  
  RESULTS
  Using the new classification system, 51 subjects were characterized as CM MPGN and 20 as IM MPGN. In the CM MPGN group, there was a non-significant trend towards lower proteinuria but higher serum creatinine values. At biopsy, most subjects had less than 50% global sclerosis or cortical scarring. The majority of subjects in the CM MPGN group (41%) had C3 nephropathy while 60% of subjects in IM MPGN group had C3 dominant disease. Treatment and outcomes: During follow-up (median 2 years), 20 patients reached a clinical end point of dialysis or death. The mean creatinine was significantly higher while the baseline proteinuria also trended slightly higher. Prednisone use was statistically higher in the survivor group.
  
  
  CONCLUSIONS
  Our study highlights the clinicopathological features of patients with biopsy proven MPGN with no known etiological factors and sheds some light on the incidence and outcomes of various categories of MPGN under the new criteria, including MPGN with "dominant C3" deposits, rapidly becoming a descriptive diagnosis.
authors.forename: Preeti
authors.initials: P
authors.lastname: Nargund
authors.forename: Neeraja
authors.initials: N
authors.lastname: Kambham
authors.forename: Kshama
authors.initials: K
authors.lastname: Mehta
authors.forename: Richard A
authors.initials: RA
authors.lastname: Lafayette
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000418:Albumins / Q000032:analysis; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001706:Biopsy / Q000379:methods; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D015922:Complement C1q / Q000032:analysis; D003176:Complement C3 / Q000032:analysis; D003404:Creatinine / Q000097:blood; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D005500:Follow-Up Studies; D015432:Glomerulonephritis, Membranoproliferative / Q000145:classification / Q000473:pathology*; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis; D007074:Immunoglobulin G / Q000032:analysis; D007075:Immunoglobulin M / Q000032:analysis; D007145:Immunoglobulin kappa-Chains / Q000032:analysis; D007146:Immunoglobulin lambda-Chains / Q000032:analysis; D007672:Kidney Cortex / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011241:Prednisone / Q000627:therapeutic use; D011507:Proteinuria / Q000652:urine; D055815:Young Adult
chemical_list: D000418:Albumins; D000893:Anti-Inflammatory Agents; D003176:Complement C3; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007145:Immunoglobulin kappa-Chains; D007146:Immunoglobulin lambda-Chains; D015922:Complement C1q; D005340:Fibrinogen; D003404:Creatinine; D011241:Prednisone