BACKGROUND, AIMS AND OBJECTIVES:
The OXFORD classification of IgA nephropathy assessed four histological features mesangial hypercellularity (M1), Endocapillary proliferation (E1), segmental sclerosis (S1) and tubular atrophy/interstitial fibrosis (T1&T2) and claimed that these features have prognostic significance. This study is limited by its exclusion of rapidly progressive cases, mild and severe forms of the disease. We in the present study focused on the application of MEST score in an Indian population in a tertiary medical centre and evaluated its significance in predicting outcome as well as disease progression. We also evaluated other pathological features apart from the MEST score which can predict the outcome and disease progression.
METHODOLOGY:
Two hundred and eighty two patients with biopsy proven IgA nephropathy were included in this study from January 2006-December 2011. We included all cases with ≥8 glomeruli, rapidly progressive cases, all ranges of proteinuria, all stages of chronic kidney disease including CKD stage 4 and 5. We separately analyzed cases with renal biopsies with 5-7 glomeruli. The association of MEST with clinical features at the time of biopsy was assessed. eGFR(estimated glomerular filtration rate) and 24 hours urine proteinuria at one year follow up, end stage renal failure at 2 years and 5 years using extrapolated eGFR, 50% reduction in eGFR and final eGFR were taken as outcomes. To determine the associations between clinical features with MEST and other pathological variables, chisquare test, independent T test and ANOVA were used. To find whether the MEST is a predictor, a binary logistic regression was done having end stage renal failure (ESRD) in extrapolated eGFR as outcome. A univariate analysis and multivariate linear regression was done with final eGFR as outcome.
RESULTS:
IgA nephropathy constituted 6.8% of total native renal biopsies. The mean of age presentation was 34.6 years. 87% of patients were presented with microscopic hematuria and 20% with nephrotic syndrome. 35.8% of patients had eGFR<30 ml/min/1.732m2 at the time of presentation. The OXFORD classification in our population was as follows M1 (10.3%), E1 (36.6%), S1 (63.1%) and T&T2 (85.5%). Histologically our patients had more chronic lesions (85.5% of patients with tubular atrophy/interstitial fibrosis) compared to OXFORD study (22%). Segmental sclerosis and tubular atrophy were seen to predict the outcome in univariate and multivariate analysis when final eGFR was taken as outcome. When ESRD and 50% reduction of eGFR were the outcome, tubular atrophy/interstitial fibrosis was the only factor predicting the outcome. MAP and proteinuria also had independent predictive value for outcome. Vascular and crescentic lesions did not have independent predictive value for outcome. Clinicopathological correlation between biopsies with average number of glomeruli ranging from 5 to 7 did not differ from those with more than 8 glomeruli.
CONCLUSIONS:
We conclude that OXFORD classification is useful in assessing the progression of the disease and tubular atrophy/interstitial fibrosis is the utmost important factor predicting the outcome in our population
