Oxford Classification of IgA nephropathy 2016: an update from the IgA Nephropathy Classification Working Group.
Since the Oxford Classification of IgA nephropathy (IgAN) was published in 2009, MEST scores have been increasingly used in clinical practice. Further retrospective cohort studies have confirmed that in biopsy specimens with a minimum of 8 glomeruli, mesangial hypercellularity (M), segmental sclerosis (S), and interstitial fibrosis/tubular atrophy (T) lesions predict clinical outcome. In a larger, more broadly based cohort than in the original Oxford study, crescents (C) are predictive of outcome, and we now recommend that C be added to the MEST score, and biopsy reporting should provide a MEST-C score. Inconsistencies in the reporting of M and endocapillary cellularity (E) lesions have been reported, so a web-based educational tool to assist pathologists has been developed. A large study showed E lesions are predictive of outcome in children and adults, but only in those without immunosuppression. A review of S lesions suggests there may be clinical utility in the subclassification of segmental sclerosis, identifying those cases with evidence of podocyte damage. It has now been shown that combining the MEST score with clinical data at biopsy provides the same predictive power as monitoring clinical data for 2 years; this requires further evaluation to assess earlier effective treatment intervention. The IgAN Classification Working Group has established a well-characterized dataset from a large cohort of adults and children with IgAN that will provide a substrate for further studies to refine risk prediction and clinical utility, including the MEST-C score and other factors.
Hospital Británico de Buenos Aires, Argentina. Electronic address: htrimarchi@hotmail.com.
Hernán
H
Trimarchi
Department of Infection, Immunity, and Inflammation, University of Leicester, Leicester, United Kingdom.
Jonathan
J
Barratt
Department of Medicine, Toronto General Research Institute, University Health Network, Toronto General Hospital, Toronto, Ontario, Canada.
Daniel C
DC
Cattran
Centre for Complement and Inflammation Research, Department of Medicine, Imperial College, London, United Kingdom.
H Terence
HT
Cook
Fondazione Ricerca Molinette, Nephrology, Dialysis, and Transplantation, Regina Margherita Hospital, Turin, Italy.
Rosanna
R
Coppo
Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Mark
M
Haas
Department of Nephrology, National Clinical Center of Kidney Disease, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China.
Zhi-Hong
ZH
Liu
Department of Cellular Pathology, Oxford University Hospitals, Oxford, United Kingdom.
Ian S D
IS
Roberts
Department of Nephrology, Fujita Health University School of Medicine, Toyoake Aichi, Japan.
Yukio
Y
Yuzawa
Renal Division, Peking University First Hospital, Beijing, China.
Hong
H
Zhang
Department of Infection, Immunity, and Inflammation, University of Leicester, Leicester, United Kingdom.
John
J
Feehally
Hospital Británico de Buenos Aires, Argentina.
D001284:Atrophy; D001706:Biopsy; D005355:Fibrosis; D005919:Glomerular Filtration Rate; D005922:Glomerulonephritis, IGA / Q000145:classification* / Q000188:drug therapy / Q000276:immunology / Q000473:pathology; D005923:Glomerulosclerosis, Focal Segmental / Q000145:classification* / Q000188:drug therapy / Q000276:immunology / Q000473:pathology; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007678:Kidney Glomerulus / Q000098:blood supply / Q000166:cytology / Q000276:immunology / Q000473:pathology*; D007684:Kidney Tubules / Q000166:cytology / Q000276:immunology / Q000473:pathology*; D050527:Mesangial Cells / Q000473:pathology; D011507:Proteinuria; D018570:Risk Assessment; D012598:Sclerosis; D016896:Treatment Outcome
D007166:Immunosuppressive Agents
IgA nephropathy; chronic kidney disease; glomerulonephritis; proteinuria