| 저자 |
Seohyun Park, Jong Hyun Jhee, Hae-Ryong Yun, Hyoungnae Kim, Jung Tak Park, Tae-Hyun Yoo, Shin-Wook Kang, Seung Hyeok Han |
| 초록 |
Objectives:
Complement activation has been highlighted in the pathogenesis of IgA nephropathy. However, it is unknown how the complement is connected to the downstream phenotype of IgA nephropathy. In this study, we investigated the association of the mesangial C3 deposits with the Oxford classification and their joint effects on the prognosis of IgA nephropathy.
Methods: We included 408 patients with biopsy-proven early stage IgA nephropathy [T0 and estimated glomerular filtration rate (eGFR) ≥30 ml/min/1.73m2] between 2009 and 2016 at Yonsei University Health System. C3 deposit was defined as the immunofluorescence intensity of C3 ≥2+ within the mesangium. The study subjects were classified according to the combination of C3 deposits and each lesion of the Oxford classification. Primary endpoint was the development of a 30% decline in eGFR during follow-up.
Results:
Among the Oxford lesions, M1 (mesangial proliferation), S1 (segmental sclerosis), and crescent were significantly correlated with C3 deposit, whereas E1 (endocapillary proliferation) was not. During a median follow-up duration of 32.5 (18.0 – 61.8) months, primary endpoint occurred in 32 patients (7.9%). In individual multivariable-adjusted analyses, the presence of M1, S1, and C3 deposit was significantly associated with increased risk of primary outcome. In combined analyses with C3 deposit and each of the Oxford lesions, HRs were significantly higher in the presence of C3/M1 and C3/S1, and C3/crescent than in the presence of each single lesion alone.
Conclusions: C3 deposit was significantly associated with the Oxford M-, S-, and crescent scores. In addition, risk of adverse renal outcome was consistently highest when C3 deposit was added to each score. These findings suggest that complement activation can strengthen the significance of the Oxford score and the presence of both components portends a poorer prognosis in IgA nephropathy
|