Validation of the Oxford classification of IgA nephropathy in cohorts with different presentations and treatments.
The Oxford Classification of IgA Nephropathy (IgAN) identified mesangial hypercellularity (M), endocapillary proliferation (E), segmental glomerulosclerosis (S), and tubular atrophy/interstitial fibrosis (T) as independent predictors of outcome. Whether it applies to individuals excluded from the original study and how therapy influences the predictive value of pathology remain uncertain. The VALIGA study examined 1147 patients from 13 European countries that encompassed the whole spectrum of IgAN. Over a median follow-up of 4.7 years, 86% received renin-angiotensin system blockade and 42% glucocorticoid/immunosuppressive drugs. M, S, and T lesions independently predicted the loss of estimated glomerular filtration rate (eGFR) and a lower renal survival. Their value was also assessed in patients not represented in the Oxford cohort. In individuals with eGFR less than 30 ml/min per 1.73 m(2), the M and T lesions independently predicted a poor survival. In those with proteinuria under 0.5 g/day, both M and E lesions were associated with a rise in proteinuria to 1 or 2 g/day or more. The addition of M, S, and T lesions to clinical variables significantly enhanced the ability to predict progression only in those who did not receive immunosuppression (net reclassification index 11.5%). The VALIGA study provides a validation of the Oxford classification in a large European cohort of IgAN patients across the whole spectrum of the disease. The independent predictive value of pathology MEST score is reduced by glucocorticoid/immunosuppressive therapy.
City of the Health and the Science of Turin Health Agency, Regina Margherita Children's Hospital, Turin, Italy.
Rosanna
R
Coppo
Hôpital du Sacré-Coeur de Montréal, Montreal, Canada.
Stéphan
S
Troyanov
Oxford University Hospitals, Oxford, UK.
Shubha
S
Bellur
Unversity Health Network, Toronto General Hospital, Toronto, Canada.
Daniel
D
Cattran
Imperial College, Hammersmith Hospital, London, UK.
H Terence
HT
Cook
University Hospitals of Leicester, Leicester, UK.
John
J
Feehally
Oxford University Hospitals, Oxford, UK.
Ian S D
IS
Roberts
Laura
L
Morando
Roberta
R
Camilla
Vladimir
V
Tesar
Sigrid
S
Lunberg
Loreto
L
Gesualdo
Francesco
F
Emma
Cristiana
C
Rollino
Alessandro
A
Amore
Manuel
M
Praga
Sandro
S
Feriozzi
Giuseppe
G
Segoloni
Antonello
A
Pani
Giovanni
G
Cancarini
Magalena
M
Durlik
Elisabetta
E
Moggia
Gianna
G
Mazzucco
Costantinos
C
Giannakakis
Eva
E
Honsova
B Brigitta
BB
Sundelin
Anna Maria
AM
Di Palma
Franco
F
Ferrario
Eduardo
E
Gutierrez
Anna Maria
AM
Asunis
Jonathan
J
Barratt
Regina
R
Tardanico
Agnieszka
A
Perkowska-Ptasinska
D000293:Adolescent; D000328:Adult; D001284:Atrophy; D002648:Child; D018450:Disease Progression; D005060:Europe; D005260:Female; D005355:Fibrosis; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate; D005920:Glomerular Mesangium / Q000473:pathology; D005922:Glomerulonephritis, IGA / Q000145:classification* / Q000188:drug therapy / Q000473:pathology*; D005923:Glomerulosclerosis, Focal Segmental / Q000473:pathology; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007668:Kidney / Q000098:blood supply / Q000473:pathology*; D007676:Kidney Failure, Chronic / Q000473:pathology* / Q000503:physiopathology; D007684:Kidney Tubules / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000473:pathology; D011237:Predictive Value of Tests; D011507:Proteinuria / Q000473:pathology; D012084:Renin-Angiotensin System / Q000187:drug effects; D012189:Retrospective Studies; D055815:Young Adult
D007166:Immunosuppressive Agents