title: 30-year follow-up study of IgA nephritis in a Southeast Asian population: an evaluation of the Oxford histological classification .
abstract: BACKGROUND
  In 1985 we reported that 11% of a cohort of 151 patients with IgA nephritis (IgAN) had developed end-stage renal disease (ESRD) after a follow-up period of 5 years. 15 years later, 35% had developed ESRD.
  
  
  METHODS
  We retrieved 125 stored renal biopsy paraffin blocks of the original cohort. From these, 102 patients were included in the present study and scored according to the Oxford classification as 21 specimens with less than 8 glomeruli were excluded and in 2 others, tissue samples were too tiny for a re-block. ESRD was ascertained by linking the study cohort to the Singapore Renal Registry at the National Registry of Diseases Office.
  
  
  RESULTS
  Renal survival curves for each of the Oxford MEST lesions: endocapillary proliferation (E) (p < 0.04), segmental glomerulosclerosis (S) (p < 0.05), tubular atrophy/interstitial fibrosis (p < 0.0001) were significantly associated with ESRD. Mesangial hypercellularity, less commonly associated with progressive chronic kidney disease (CKD) in the study, was independently associated with ESRD at 30 years (p < 0.03). In this cohort, E and S were associated with lower eGFR at presentation and doubling of serum creatinine in the first 5 years. This study's initial 5 years was representative of the "natural history" of IgAN since no renin-angiotensin system (RAS) blockers or immunosuppression were administered. This represents the early phase of disease progression. E and S may be considered "early disease activity predictors".
  
  
  CONCLUSIONS
  Mesangial hypercellularity and tubular atrophy/interstitial fibrosis (M1 and T1/T2 lesion) of the Oxford classification independently predicted long term ESRD. .
authors.forename: Keng Thye
authors.initials: KT
authors.lastname: Woo
authors.forename: Cynthia C
authors.initials: CC
authors.lastname: Lim
authors.forename: Marjorie W Y
authors.initials: MW
authors.lastname: Foo
authors.forename: Hwai L
authors.initials: HL
authors.lastname: Loh
authors.forename: Ai Zhen
authors.initials: AZ
authors.lastname: Jin
authors.forename: Yok Mooi
authors.initials: YM
authors.lastname: Chin
authors.forename: Jason C J
authors.initials: JC
authors.lastname: Choo
authors.forename: Puay Hoon
authors.initials: PH
authors.lastname: Tan
authors.forename: Khuan Yew
authors.initials: KY
authors.lastname: Chow
authors.forename: Lina H L
authors.initials: LH
authors.lastname: Choong
authors.forename: Han Khim
authors.initials: HK
authors.lastname: Tan
authors.forename: Kok Seng
authors.initials: KS
authors.lastname: Wong
authors.forename: Choong Meng
authors.initials: CM
authors.lastname: Chan
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001284:Atrophy / Q000473:pathology; D002196:Capillaries / Q000473:pathology; D049109:Cell Proliferation; D018450:Disease Progression; D042783:Endothelial Cells; D005260:Female; D005355:Fibrosis; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate; D005922:Glomerulonephritis, IGA / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D005923:Glomerulosclerosis, Focal Segmental / Q000473:pathology; D006801:Humans; D007676:Kidney Failure, Chronic / Q000209:etiology / Q000473:pathology*; D007678:Kidney Glomerulus / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D012846:Singapore