TY - JOUR
T1 - Poor renal outcomes in patients with anti-neutrophil cytoplasmic antibody-associated crescentic glomerulonephritis and normal renal function at diagnosis
AU - Hanaoka, Hironari
AU - Ota, Yuichiro
AU - Takeuchi, Tsutomu
AU - Kuwana, Masataka
N1 - Funding Information:
H.H. received consulting fees from AstraZeneca. T.T. received grants from Abbott, Astellas, Bristol-Myers, Chugai, Daiichi Sankyo, Eisai, Mitsubishi Tanabe, Pfizer, Sanofi, Santen, Takeda, Teijin, AbbVie, Asahi Kasei, and Taisho Toyama; lecture fees from Abbott, Bristol-Myers, Chugai, Eisai, Janssen, Mitsubishi Tanabe, Pfizer, Takeda, Astellas, and Daiichi Sankyo; and consulting fees from AstraZeneca, Eli Lilly, Novartis, Mitsubishi Tanabe, Asahi Kasei, AbbVie, and Daiichi Sankyo.
Publisher Copyright:
© 2016, International League of Associations for Rheumatology (ILAR).
PY - 2016/2/1
Y1 - 2016/2/1
N2 - The aim of this study is to investigate the renal outcomes of anti-neutrophil cytoplasmic antibody (ANCA)-associated crescentic glomerulonephritis in patients with normal estimated glomerular filtration rate (eGFR) at diagnosis. Twenty-seven patients with biopsy-proven ANCA-associated crescentic glomerulonephritis were retrospectively recruited and were divided into 12 with normal eGFR (≥60 ml/min/1.73 m2) and 15 with low eGFR (<60 ml/min/1.73 m2) at baseline. Clinical and renal pathological findings at diagnosis and renal outcomes for up to 3 years were compared between the two groups. Two patients in the low eGFR group died of severe bacterial pneumonia. In the normal eGFR group, the following characteristics were observed: younger age at diagnosis (p = 0.04), diagnosis of granulomatosis polyangiitis (GPA) (p < 0.01), and lower frequency of cyclophosphamide treatment (p = 0.03). On renal pathological analysis, the normal eGFR group had a significantly lower proportion of cellular crescent formation (p = 0.01), fibrinoid necrosis (p = 0.01), interstitial fibrosis (p = 0.02), and tubular atrophy (p = 0.02). As a result, the two groups did not significantly differ in remission rates, relapse rates, Birmingham vasculitis score, vasculitis damage index, or eGFR on 3-year follow-up. Patients with biopsy-proven ANCA-associated glomerulonephritis and normal eGFR at diagnosis have poor renal outcomes and may require standard intensive immunosuppressive treatment to prevent accrual of damage.
AB - The aim of this study is to investigate the renal outcomes of anti-neutrophil cytoplasmic antibody (ANCA)-associated crescentic glomerulonephritis in patients with normal estimated glomerular filtration rate (eGFR) at diagnosis. Twenty-seven patients with biopsy-proven ANCA-associated crescentic glomerulonephritis were retrospectively recruited and were divided into 12 with normal eGFR (≥60 ml/min/1.73 m2) and 15 with low eGFR (<60 ml/min/1.73 m2) at baseline. Clinical and renal pathological findings at diagnosis and renal outcomes for up to 3 years were compared between the two groups. Two patients in the low eGFR group died of severe bacterial pneumonia. In the normal eGFR group, the following characteristics were observed: younger age at diagnosis (p = 0.04), diagnosis of granulomatosis polyangiitis (GPA) (p < 0.01), and lower frequency of cyclophosphamide treatment (p = 0.03). On renal pathological analysis, the normal eGFR group had a significantly lower proportion of cellular crescent formation (p = 0.01), fibrinoid necrosis (p = 0.01), interstitial fibrosis (p = 0.02), and tubular atrophy (p = 0.02). As a result, the two groups did not significantly differ in remission rates, relapse rates, Birmingham vasculitis score, vasculitis damage index, or eGFR on 3-year follow-up. Patients with biopsy-proven ANCA-associated glomerulonephritis and normal eGFR at diagnosis have poor renal outcomes and may require standard intensive immunosuppressive treatment to prevent accrual of damage.
KW - ANCA-associated glomerulonephritis
KW - Normal estimated glomerular filtration rate
KW - Prognosis
KW - Vasculitis
UR - http://www.scopus.com/inward/record.url?scp=84958170132&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84958170132&partnerID=8YFLogxK
U2 - 10.1007/s10067-015-3162-0
DO - 10.1007/s10067-015-3162-0
M3 - Article
C2 - 26742758
AN - SCOPUS:84958170132
SN - 0770-3198
VL - 35
SP - 495
EP - 500
JO - Clinical Rheumatology
JF - Clinical Rheumatology
IS - 2
ER -