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• W2152853007 abstract "IgA nephropathy is the most common glomerular disease worldwide, yet there is no international consensus for its pathological or clinical classification. Here a new classification for IgA nephropathy is presented by an international consensus working group. The goal of this new system was to identify specific pathological features that more accurately predict risk of progression of renal disease in IgA nephropathy, thus enabling both clinicians and pathologists to improve individual patient prognostication. In a retrospective analysis, sequential clinical data were obtained on 265 adults and children with IgA nephropathy who were followed for a median of 5 years. Renal biopsies from all patients were scored by pathologists blinded to the clinical data for pathological variables identified as reproducible by an iterative process. Four of these variables: (1) the mesangial hypercellularity score, (2) segmental glomerulosclerosis, (3) endocapillary hypercellularity, and (4) tubular atrophy/interstitial fibrosis were subsequently shown to have independent value in predicting renal outcome. These specific pathological features withstood rigorous statistical analysis even after taking into account all clinical indicators available at the time of biopsy as well as during follow-up. The features have prognostic significance and we recommended they be taken into account for predicting outcome independent of the clinical features both at the time of presentation and during follow-up. The value of crescents was not addressed due to their low prevalence in the enrolled cohort. IgA nephropathy is the most common glomerular disease worldwide, yet there is no international consensus for its pathological or clinical classification. Here a new classification for IgA nephropathy is presented by an international consensus working group. The goal of this new system was to identify specific pathological features that more accurately predict risk of progression of renal disease in IgA nephropathy, thus enabling both clinicians and pathologists to improve individual patient prognostication. In a retrospective analysis, sequential clinical data were obtained on 265 adults and children with IgA nephropathy who were followed for a median of 5 years. Renal biopsies from all patients were scored by pathologists blinded to the clinical data for pathological variables identified as reproducible by an iterative process. Four of these variables: (1) the mesangial hypercellularity score, (2) segmental glomerulosclerosis, (3) endocapillary hypercellularity, and (4) tubular atrophy/interstitial fibrosis were subsequently shown to have independent value in predicting renal outcome. These specific pathological features withstood rigorous statistical analysis even after taking into account all clinical indicators available at the time of biopsy as well as during follow-up. The features have prognostic significance and we recommended they be taken into account for predicting outcome independent of the clinical features both at the time of presentation and during follow-up. The value of crescents was not addressed due to their low prevalence in the enrolled cohort. IgA nephropathy (IgAN) is the commonest glomerular disease worldwide, yet there is no international consensus for its pathological or clinical classification. Nephrologists use clinical information to identify the risk of developing progressive chronic kidney disease in individual patients with IgAN. There is now extensive evidence that a number of clinical features at presentation predict risk of progressive chronic kidney disease. In published series, these consistently include extent of proteinuria, hypertension, and excretory renal function.1.D’Amico G. Natural history of idiopathic IgA nephropathy and factors predictive of disease outcome.Semin Nephrol. 2004; 24: 179-196Abstract Full Text Full Text PDF PubMed Scopus (343) Google Scholar, 2.Donadio J.V. Bergstralh E.J. Grande J.P. et al.Proteinuria patterns and their association with subsequent end-stage renal disease in IgA nephropathy.Nephrol Dial Transplant. 2002; 17: 1197-1203Crossref PubMed Scopus (139) Google Scholar, 3.Ibels L.S. Gyory A.Z. IgA nephropathy: analysis of the natural history, important factors in the progression of renal disease, and a review of the literature.Medicine (Baltimore). 1994; 73: 79-102Crossref PubMed Scopus (216) Google Scholar, 4.Nicholls K.M. Fairley K.F. Dowling J.P. et al.The clinical course of mesangial IgA associated nephropathy in adults.Q J Med. 1984; 53: 227-250PubMed Google Scholar, 5.Woo K.T. Edmondson R.P. Wu A.Y. et al.The natural history of IgA nephritis in Singapore.Clin Nephrol. 1986; 25: 15-21PubMed Google Scholar Recent work also indicates the prognostic importance of reduction in proteinuria during follow-up, allowing continuing refinement of the prognostic information given to an individual patient.6.Reich H.N. Troyanov S. Scholey J.W. et al.Remission of proteinuria improves prognosis in IgA nephropathy.J Am Soc Nephrol. 2007; 18: 3177-3183Crossref PubMed Scopus (358) Google Scholar Pathologists have developed a number of classifications of IgAN over the last 25 years; some are semiquantitative,7.Alamartine E. Sabatier J.C. Berthoux F.C. Comparison of pathological lesions on repeated renal biopsies in 73 patients with primary IgA glomerulonephritis: value of quantitative scoring and approach to final prognosis.Clin Nephrol. 1990; 34: 45-51PubMed Google Scholar, 8.Radford Jr, M.G. Donadio Jr, J.V. Bergstralh E.J. et al.Predicting renal outcome in IgA nephropathy.J Am Soc Nephrol. 1997; 8: 199-207PubMed Google Scholar, 9.Katafuchi R. Kiyoshi Y. Oh Y. et al.Glomerular score as a prognosticator in IgA nephropathy: its usefulness and limitation.Clin Nephrol. 1998; 49: 1-8PubMed Google Scholar, 10.Churg J. Sobin L.H. Renal Disease, Classification and Atlas of Glomerular Disease. Igaku-Shoin, Tokyo1982Google Scholar others are single-grade classifications.11.Lee S.M. Rao V.M. Franklin W.A. et al.IgA nephropathy: morphologic predictors of progressive renal disease.Hum Pathol. 1982; 13: 314-322Abstract Full Text PDF PubMed Scopus (256) Google Scholar, 12.Haas M. Histologic subclassification of IgA nephropathy: a clinicopathologic study of 244 cases.Am J Kidney Dis. 1997; 29: 829-842Abstract Full Text PDF PubMed Scopus (381) Google Scholar, 13.Wakai K. Kawamura T. Endoh M. et al.A scoring system to predict renal outcome in IgA nephropathy: from a nationwide prospective study.Nephrol Dial Transplant. 2006; 21: 2800-2808Crossref PubMed Scopus (112) Google Scholar, 14.Manno C. Strippoli G.F. D′Altri C. et al.A novel simpler histological classification for renal survival in IgA nephropathy: a retrospective study.Am J Kidney Dis. 2007; 49: 763-775Abstract Full Text Full Text PDF PubMed Scopus (113) Google Scholar, 15.Coppo R. Schena F.P. IgA nephropathies.in: Davison A.M. Ritz E. Cameron J.S. Winearls C. Oxford Textbook of Clinical Nephrology. 3rd edn. Oxford University Press, Oxford, UK2005Google Scholar Each of these classifications has been developed from expert opinion, each has strengths and limitations in predicting prognosis, and none has gained pre-eminence. There is continuing debate whether pathological features seen on renal biopsy contribute additional prognostic information beyond that provided by clinical features.16.Bartosik L.P. Lajoie G. Sugar L. et al.Predicting progression in IgA nephropathy.Am J Kidney Dis. 2001; 38: 728-735Abstract Full Text Full Text PDF PubMed Scopus (293) Google Scholar This lack of consensus on classifications based on pathology has weakened a number of areas of investigation into IgAN. It has contributed to slow progress in developing a prognostic system with the sensitivity and specificity to predict outcome for individual patients. It has reduced the capacity to make international comparisons between different outcome studies, and it has limited opportunities to refine the stratification of risk for the design of clinical intervention trials. This is a major disadvantage in a slowly progressive disease like IgAN where large studies of long duration are needed to evaluate new interventions unless patients with a high risk of progression can be better defined early in the course of the disease. In 2004, a proposal to develop a consensus clinicopathological classification came from the International IgA Nephropathy Network—an informal network of nephrologists and scientists with representation from the majority of nephrology research groups around the world active in the field of IgAN (www.IgAN-world.org)—and members of the Renal Pathology Society interested in IgAN. A questionnaire among renal pathologists showed support for the development of a consensus classification of IgAN provided it could be shown to have real clinical utility. Therefore, representatives of the International IgA Nephropathy Network and the Renal Pathology Society established a working group to seek agreement on an evidence-based clinicopathological consensus classification for IgAN.17.Feehally J. Barratt J. Coppo R. et al.International IgA nephropathy network clinico-pathological classification of IgA nephropathy.Contrib Nephrol. 2007; 157: 13-18PubMed Google Scholar From the beginning this was designed as an international consensus aiming to involve nephrologists and pathologists from as many parts of the world as possible, including all areas where IgAN is known to be of high prevalence. Eventually, the consensus group had representation from 10 countries on four continents. The goal of the new classification was to identify specific pathological features that more accurately predict risk of progression of renal disease in IgAN, which would enable both clinicians and pathologists to improve individual patient prognostication. It was recognized that such a classification may also in the future facilitate the identification of specific features that may predict response to immunosuppression or other specific treatments, and refine recruitment to clinical trials by their capacity to stratify patients by their risk of progression. The work was approached without preconceptions to test objectively the predictive power of a wide range of pathological features. The consensus work required unity of purpose and a collaborative approach. Organizational challenges included the development of tools allowing consistent data collection, and the need to meet the varying requirements of institutional review boards and ethics committees so that anonymized pathological material and clinical data could be circulated within and beyond its country of origin. The overall approach used by the working group was the following:•Agreement on a clinical data set useful for outcome studies in IgAN;•Identification of centers willing to provide cases with sufficient clinical data and biopsy material available for review, including cohorts varying in age, and in geographical and racial origin;•Agreement on definitions and scoring of a wide range of pathological features;•Testing reproducibility between pathologists of scoring these features; and•Analysis of informative pathological features in the context of clinical outcome to develop a classification. By this rigor of approach, we aimed to gain the confidence of clinicians and investigators worldwide, so that the new classification will become the norm in routine clinical practice and in future clinicopathological outcome reports of IgAN. The working group had two consensus meetings in 2005 and 2008, both held in Oxford, UK. It has, therefore, been decided to call the product of our work, the Oxford Classification of IgA Nephropathy. Clinical data and adequate renal biopsy material from 265 patients with IgAN were collected from eight countries on four continents. Five centers from Asia, six from Europe, two from United States, one from South America, and two multicenter networks (Canada and USA) participated in the study (Table 1). The proportion of children was similar in each continent (~30%).Table 1Age and geographical origin of the study cohort of 265 cases of IgA nephropathyAdultsChildren (age<18 years at biopsy)Total26520659Asia4814 ChinaBeijing122Hong Kong91Nanjing71 JapanTokyo191Wakayama19Europe7321 FranceSt Etienne231 ItalyBari231Milano163Roma–9Torino37 United KingdomGlasgow8–North America8224 CanadaToronto320 United StatesBirmingham121Mayo Clinic144South West Study Group2419South America30 ChileSantiago30 Open table in a new tab Pathology information was complete for each variable in all 265 cases. There were a median number of 18 glomeruli per biopsy (interquartile range 8–24). Distributions of selected pathology findings are shown in Figure 1. In all, 42 and 45% of patients had endocapillary hypercellularity or crescents (but the median numbers of glomeruli involved in each affected patient were only 12 and 9%, respectively). Necrosis was seen in only six cases and glomerular basement membrane duplication in 30 cases. The majority of patients had no arterial or arteriolar lesions. The reproducibility of the various pathological lesions is described in detail in the accompanying paper (Roberts et al., The Oxford Classification of IgA Nephropathy pathology definitions, correlations and reproducibility).18.Roberts I.S.D. Cook T. Troyanov S. The Oxford classification of IgA Nephropathy: Pathology definitions, correlations and reproducibility.Kidney Int. 2009Abstract Full Text Full Text PDF Scopus (651) Google Scholar Following refinement of the definitions, those pathological lesions that continued to show poor reproducibility within the working group were not incorporated into the final classification, as even lower reproducibility could be expected in routine practice without the advantage of the iterative processes of the working group. These included the percentage of normal glomeruli as well as the percentage of glomeruli showing adhesions, glomerular basement membrane duplication, necrosis, arteriolar lesions, and interstitial inflammation involving non-fibrotic cortex. Reproducibility of scoring for adhesions increased when combined with segmental sclerosis, suggesting that different pathologists identified the same lesion as either segmental sclerosis or an adhesion. For subsequent analysis, segmental sclerosis and adhesions were summed. Details of the correlations between the different pathology variables are presented in the accompanying paper (Roberts et al.). For those variables that displayed considerable correlation (r>0.8), it was decided to include only one variable from each group for further consideration based on reproducibility, ease of identification, and susceptibility to sampling error. The mesangial hypercellularity score was preferred to the percentage of glomeruli showing severe mesangial hypercellularity as it is more reproducible. A simplification of the mesangial hypercellularity score to <50 or >50% showing mesangial hypercellularity is described in the accompanying paper. The percentage of glomeruli showing cellular and fibrocellular crescents was preferred to the crescent score, which required a complex calculation including scoring the size of the crescents in each glomerulus. Interstitial fibrosis combined with tubular atrophy was preferred to global glomerulosclerosis, as its quantification is less susceptible to error due to paucity of glomeruli or subcapsular sampling, whichever was the higher value (interstitial fibrosis or tubular atrophy) chosen. The highest arterial score for any size of vessel was preferred to either the arcuate or interlobular artery score as it was less susceptible to sampling error. Therefore, the selected pathology variables used in the subsequent analysis were the following:mesangial hypercellularity score;segmental glomerulosclerosis or adhesion;endocapillary hypercellularity;cellular only and cellular or fibrocellular crescents;tubular atrophy/interstitial fibrosis; andartery score. The independent predictive value of the continuous glomerular variables could not be easily studied using multivariate linear analysis in light of severely skewed distributions. Therefore, receiver operating characteristic curves were drawn for each variable to determine the optimal cutoffs predicting a worse outcome (the most clinically relevant outcome was the rate of renal function decline, which we needed to dichotomize to perform this analysis). The optimal cutoff for the mesangial hypercellularity score was 0.71. This number was approximated to 0.5 (without significant loss of sensitivity) to facilitate scoring. Segmental glomerulosclerosis, endocapillary hypercellularity, and extracapillary proliferation were categorized as either present or absent as determined by receiver operating characteristic curve. Tubular atrophy/interstitial fibrosis was classified as absent (0%), mild (1–25%), moderate (26–50%), or severe (>50%), because this straightforward reproducible classification is widely used in clinical practice. Clinical features at the time of biopsy and during follow-up are shown in Table 2 and are typical of IgAN. At the time of renal biopsy, the median age was 32 years (4–73 years), with male predominance. The mean arterial pressure (MAP) was 98±18 mm Hg (63% of adult patients had blood pressure above the value of 130/80 mm Hg and 31% were taking antihypertensive medication). Nine children (15%) had adjusted blood pressure >130/80 mm Hg (MAP s.d. score >1) or were taking antihypertensive medication. The estimated glomerular filtration rate (eGFR) values were evenly distributed within stages 1, 2, and 3 of the Kidney Disease Outcomes Quality Initiative (KDOQI) classification of chronic kidney disease, although most children had stage 1 chronic kidney disease (77%). Median proteinuria was 1.7 g per 24 h (1.95 g per 24 h per 1.73 m2 in children). Median follow-up was 5 years (range: 1–22 years, with 90% followed for more than 3 years). Twenty-nine percentage of the patients enrolled (47% of children and 23% of adults) received immunosuppressive therapy, consisting of variable dosages of corticosteroids with additional immunosuppressive agents in only 9% of the cases. Patients with segmental glomerulosclerosis, tubular atrophy/interstitial fibrosis, and arterial lesions were more likely to have been treated with renin-angiotensin system blockade (RAS) blockade (angiotensin-converting enzyme inhibitor or angiotensin receptor blocker). Conversely, those with endocapillary or extracapillary lesions received more immunosuppressive treatment (Table 3). Fish oil was prescribed for 16% and statins for 13% of the patients. No patient had a tonsillectomy during the follow-up.Table 2Clinical characteristics at the time of biopsy and follow-up in 265 patients with IgA nephropathyAt time of biopsyFollow-upAge (years)30 (4–73)Duration of follow-up (months)69 (12–268)Female28%Pediatric at time of biopsy (<18 years)22%Ethnicity (Caucasian/African/Asian/Other)66, 3, 27, and 4%BMI25±6MAP (mm Hg)98±17MAP (mm Hg)95±10Taking antihypertensive medication31%No. of antihypertensive medications0.9 (0–4.7)Treated with RAS blockade20%Treated with RAS blockade (ACEi and ARB)74% (68 and 22%)eGFR (ml/min per 1.73 m2)83±36Rate of renal function decline (ml/min per 1.73 m2 per year)-3.5±8.4Stage 1, 2, 3 CKD (KDOQI)36, 38, and 26%50% Decline in renal function22%End-stage renal disease (<15 ml/min per 1.73 m2)13%Proteinuria (g/day)1.7 (0.5–18.5)Proteinuria (g/day)1.1 (0.1–9.3)Previous macroscopic hematuria34%Previous immunosuppression14%Immunosuppression29% Prednisone29% Other (cyclophosphamide)9% (6%)Previous use of fish oil6%Known previous tonsillectomy6%ACEi, angiotensin-converting inhibitor; ARB, angiotensin receptor blocker; BMI, body mass index; BP, blood pressure; eGFR, estimated glomerular filtration rate; MAP, mean arterial pressure; RAS, renin-angiotensin system.Values are expressed as mean±s.d. or median (range). Calculation of MAP, eGFR, and proteinuria is detailed in the text.eGFR, MAP, and proteinuria at onset were missing in 12% of cases. The median numbers of BP, GFR, and proteinuria measurements per patient were 7, 7, and 6, respectively. Open table in a new tab Table 3Therapy received during follow-up in relation to pathological features% RAS blockadeP-value% ImmunosuppressionP-valueMesangial hypercellularity score ≤0.57121 >0.575>0.130>0.1Segmental glomerulosclerosis Absent54<0.00128>0.1 Present8129Endocapillary hypercellularity Absent7617 Present72>0.145<0.001Extracapillary hypercellularity Absent72200.002 Present78>0.139Tubular atrophy/interstitial fibrosis Absent480.00331>0.1 1–25%7628 26–50%8424 >50%8550Artery score Absent680.0432>0.1 Mild8324 Moderate8619 Severe7550Percentage of patients with each pathological feature receiving renin–angiotensin system blockade or immunosuppressive therapy. Open table in a new tab ACEi, angiotensin-converting inhibitor; ARB, angiotensin receptor blocker; BMI, body mass index; BP, blood pressure; eGFR, estimated glomerular filtration rate; MAP, mean arterial pressure; RAS, renin-angiotensin system. Values are expressed as mean±s.d. or median (range). Calculation of MAP, eGFR, and proteinuria is detailed in the text. eGFR, MAP, and proteinuria at onset were missing in 12% of cases. The median numbers of BP, GFR, and proteinuria measurements per patient were 7, 7, and 6, respectively. Percentage of patients with each pathological feature receiving renin–angiotensin system blockade or immunosuppressive therapy. The mean rate of renal function decline was -3.5±8.4 ml/min per 1.73 m2 per year (–3.7±6.6 in adults and –2.7±1.05 in children, P>0.1). The end point of 50% decline in eGFR was reached in 22% of the cases and end-stage renal disease (ESRD) was reached in 13%. This was a typical cohort of patients with IgAN as indicated by the strong association observed between initial eGFR, MAP, and proteinuria as well as follow-up MAP and proteinuria and the outcomes measured (data not shown). Mesangial score, segmental glomerulosclerosis, endocapillary hypercellularity, and extracapillary proliferation were strongly associated with proteinuria at the time of biopsy. Segmental glomerulosclerosis was associated with reduced eGFR and higher MAP at the time of biopsy. Tubular atrophy/interstitial fibrosis was associated with a reduced initial eGFR and higher initial MAP and proteinuria. Arterial disease was strongly associated with initial blood pressure and eGFR but had no relation with initial proteinuria (Table 4).Table 4Correlations between pathological features and clinical features at the time of renal biopsyMAPGFRProteinuriamm HgP-valueml/min per 1.73 m2P-valueg/dayP-valueMesangial hypercellularity score≤0.5100±18>0.184±28>0.11.4 (0.6–9.2)0.001Mesangial hypercellularity score >0.598±1782±382.0 (0.5–18.5)No endocapillary hypercellularity101±190.00876±310.0011.5 (0.5–11.3)0.01Any endocapillary hypercellularity95±1592±402.0 (0.5–18.5)No extracapillary proliferation98±17>0.184±37>0.11.5 (0.5–18.5)0.002Any extracapillary proliferation98±1880±352.2 (0.5–12.0)No segmental glomerulosclerosis94±160.0495±400.0031.5 (0.5–7.2)0.004Any segmental glomerulosclerosis100±1879±341.9 (0.6–18.5)Tubular atrophy and interstitial fibrosis None (0%)91±170.03109±35<0.0011.5 (0.5–7.2)0.03 Mild (1–25%)99±1886±351.7 (0.5–18.5) Moderate (26–50%)100±1259±171.8 (0.6–7.5) Severe (≥51%)105±2446±273.0 (1.1–9.0)Artery score Absent96±170.0292±40<0.0011. 8 (0.5–18.5)>0.1 Mild104±1567±191.5 (0.6–4.6) Moderate101±2070±251.6 (0.8–7.3) Severe102±772±331.7 (1.1–2.2)GFR, glomerular filtration rate; MAP, mean arterial pressure.Mean±s.d., median (range). Open table in a new tab GFR, glomerular filtration rate; MAP, mean arterial pressure. Mean±s.d., median (range). By univariate analysis, the rate of renal function decline as well as survival without ESRD or 50% reduction in initial eGFR were significantly associated with a mesangial hypercellularity score >0.5, presence of segmental glomerulosclerosis, and tubular atrophy/interstitial fibrosis. As the outcome in patients with absent tubular atrophy/interstitial fibrosis was identical to the 1–25% group, we merged these two categories to maximize statistical power (Table 5).Table 5Correlations between pathological features and outcomes: univariate and multivariate pathologic determinants of slopeRate of renal function decline (linear regression)Survival from renal failure or a 50% drop in GFR (Cox regression)Univariate slopeMultivariateaModel A: multivariate with three pathological features + initial GFR, MAP, proteinuria. Model B: multivariate with three pathological features + initial GFR and follow-up MAP and proteinuria.Univariate hazard ratioMultivariateaModel A: multivariate with three pathological features + initial GFR, MAP, proteinuria. Model B: multivariate with three pathological features + initial GFR and follow-up MAP and proteinuria.(ml/min per 1.73 m2 per year)Model AModel B(95% CI)Model AModel Bβ (s.d.)β (s.d.)Mesangial hypercellularity score ≤0.5-0.5±3.3-2.2 (1.3)-0.8 (1.2)0.06 (0.01–0.45)0.07 (0.01–0.53)0.11 (0.01–0.80) >0.5-4.2±9.0111P<0.001P=0.10P>0.1P=0.006P=0.01P=0.03Segmental glomerulosclerosis Absent-0.5±7.5111 Present-4.4±8.4-3.6 (1.3)-2.5 (1.1)3.1 (1.4–7.3)1.8 (0.6–5.3)2.5 (0.9–7.3)P=0.001P=0.005P=0.03P=0.009P>0.1P=0.09Tubular atrophy/interstitial fibrosisbOutcomes with 0% tubular atrophy/interstitial fibrosis were identical to 1–25% tubular atrophy/interstitial fibrosis, hence the two categories were combined to maximize statistical power. 0–25%-2.5±7.6-5.2 (1.1)-3.7 (1.0)111 26–50%-5.7±8.83.5 (1.9–6.5)6.0 (2.7–13.9)5.0 (2.3–11.1) >50%-11.1±12.615.5 (7.5–31.9)17.3 (5.9–50.9)8.8 (2.9–26.4)P<0.001P<0.001P<0.001P<0.001P<0.001P<0.001CI, confidence interval; GFR, glomerular filtration rate; MAP, mean arterial pressure.Endocapillary, extracapillary, and arterial lesions were not associated with the rate of renal function decline or survival from renal failure or a 50% drop in GFR (see text, Correlations between pathological lesions and outcome).a Model A: multivariate with three pathological features + initial GFR, MAP, proteinuria. Model B: multivariate with three pathological features + initial GFR and follow-up MAP and proteinuria.b Outcomes with 0% tubular atrophy/interstitial fibrosis were identical to 1–25% tubular atrophy/interstitial fibrosis, hence the two categories were combined to maximize statistical power. Open table in a new tab CI, confidence interval; GFR, glomerular filtration rate; MAP, mean arterial pressure. Endocapillary, extracapillary, and arterial lesions were not associated with the rate of renal function decline or survival from renal failure or a 50% drop in GFR (see text, Correlations between pathological lesions and outcome). In the whole patient group, endocapillary and extracapillary proliferative lesions were not significantly predictive of the rate of renal function decline, nor of survival from a combined event. Patients with endocapillary hypercellularity deteriorated at a rate of -3.8±10.6 ml/min per 1.73 m2 per year compared with -3.3±6.4 in those without these lesions (P>0.1) and those with extracapillary proliferation deteriorated by -4.4±10.4 ml/min per 1.73 m2 per year compared with -2.8±6.3 in those without (P>0.1, with similar results when addressing cellular crescents alone). However, there was a significant interaction between endocapillary hypercellularity and immunosuppression (see below). The rate of renal function decline was almost identical in the different artery score groups (data not shown). Two models of multivariate analysis were calculated. The first model was designed to address whether the biopsy findings predicted long-term outcome independently of the initial assessment; it considered the pathology variables in addition to the initial clinical data set (eGFR, MAP and proteinuria). The second model was designed to address which of the selected pathology variables were independent predictors of outcome even when clinical follow-up data were taken into account; this model included pathology data, initial eGFR, and follow-up data (MAP and proteinuria). Linear regression of rate of renal function decline correlated with segmental glomerulosclerosis and tubular atrophy/interstitial fibrosis in both models. The mesangial hypercellularity score failed to attain independent significance in both models. When the end points of ESRD or 50% reduction in eGFR was considered as the outcome, the Cox regression showed for both models significant associations for mesangial hypercellularity score and tubular atrophy/interstitial fibrosis, whereas the association for segmental glomerulosclerosis failed to reach statistical significance in both models. There was a marked reduction in the mean hazard ratio from 1 (with mesangial hypercellularity score >0.5) to 0.11 (an 89% reduction) when the score was ≤0.5. There was a rapid escalation of the hazard ratio as tubular atrophy/interstitial fibrosis increased: mean hazard ratio 5 (when 26–50%) and 8.8 (when >50%). The presence of endocapillary and extracapillary lesions, and the severity of arterial lesions were not statistically associated with a decreased survival from a combined event (data not shown). There was a highly significant association by univariate analysis between follow-up proteinuria and the mesangial hypercellularity score, the presence of segmental glomerulosclerosis or adhesions, and tubular atrophy/interstitial fibrosis; their association with follow-up proteinuria persisted even when adjusted for the initial proteinuria, GFR, or MAP (data not shown). Finally, odds ra" @default.
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• W2152853007 title "The Oxford classification of IgA nephropathy: rationale, clinicopathological correlations, and classification" @default.
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