Pathology and Renal Outcome of IgA Nephropathy.
10.3904/kjm.2015.88.4.397
- Author:
Jun Young LEE
1
;
Jae Won YANG
;
Jae Seok KIM
;
Young Sub KIM
;
Hyeoncheol PARK
;
Moon Hee CHAE
;
Seung Ok CHOI
;
Minseob EOM
;
Byoung Geun HAN
Author Information
1. Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea. neptune@yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
IgA nephropathy;
Prognosis;
Oxford classification;
Electron microscopy
- MeSH:
Biopsy;
Classification;
Creatinine;
Fibrosis;
Foot;
Glomerular Basement Membrane;
Glomerular Filtration Rate;
Glomerulonephritis, IGA*;
Humans;
Kidney Failure, Chronic;
Microscopy, Electron;
Pathology*;
Prognosis;
Proteinuria;
Sclerosis;
World Health Organization
- From:Korean Journal of Medicine
2015;88(4):397-405
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND/AIMS: The Oxford classification of immunoglobulin A nephropathy (IgAN) is a pathology-based prognostic classification system. However, further study is needed to determine its validity. We studied the relationships between the Oxford classification and established prognostic factors and renal survival. We also examined associations between electron microscopy findings and these parameters. METHODS: We reviewed and reclassified 213 patients who were diagnosed with IgAN from 1997 to 2007 using the Oxford and World Health Organization (WHO) classification systems. The patients were also categorized by a pathologist using electron microscopy findings, including foot process fusion, glomerular basement membrane thickness, and electron-dense deposits. We examined the correlations between light and electron microscopy data and known prognostic factors (e.g., age, sex, proteinuria, serum creatinine, estimated glomerular filtration rate [eGFR], and blood pressure). The same procedure was applied to renal survival. RESULTS: Patient age increased with the grades of segmental sclerosis (S) and tubular atrophy/interstitial fibrosis (T) (P < 0.05). eGFR decreased significantly with increasing mesangial hypercellularity (M) (p = 0.0034), S (p = 0.0003), endocapillary hypercellularity (E) (p = 0.0411), and T (P < 0.0001). MSET differed significantly by sex (P < 0.0001). The 24-h urine protein/creatinine ratio increased significantly with the degrees of S (p = 0.036), E (p = 0.0155), and T (p = 0.015). The serum creatinine level was significantly higher in patients with T2 than T1 or T0 (P < 0.0001). At the time of biopsy, the degree of tubular atrophy/interstitial fibrosis affected the doubling of serum creatinine or end-stage renal disease. However, the electron microscopy findings did not predict the renal outcome. CONCLUSIONS: Our study suggests that tubular atrophy/interstitial fibrosis is significantly associated with proteinuria and renal progression in IgAN.
