TY - JOUR
T1 - Glomerural crescent formation in renal amyloidosis
T2 - A clinicopathological study and demonstration of upregulated cell-mediated immunity
AU - Masutani, K.
AU - Nagata, M.
AU - Ikeda, H.
AU - Takeda, K.
AU - Katafuchi, R.
AU - Hirakata, H.
AU - Tsuruya, K.
AU - Iida, M.
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2008/12
Y1 - 2008/12
N2 - Background: Several studies examined glomerular crescents associated with renal amyloidosis. However, the incidence of crescents, the association between the 2 lesions, treatment and outcome are still controversial. Patients and methods: We studied 107 consecutive biopsies of renal amyloidosis, and found cellular or fibrocellular crescents in 13 cases (12.1%). We investigated the clinical characteristics, pathological findings, treatment and outcome. We also performed immunohistochemical staining using T cell, macrophage and osteopontin (OPN) markers. Results: Amyloid was of the AA type in 12 cases, and all patients had rheumatoid arthritis. Six cases with AA amyloidosis had crescentic glomerulonephritis (CrGN), and 5 presented with rapidly progressive glomerulonephritis (RPGN). The percentage of crescents correlated negatively with serum albumin (r = -0.83, p < 0.001), and positively with serum creatinine (r = 0.72, p < 0.01) and urinary protein excretion (r = 0.85, p < 0.001). All RPGN patients developed end-stage renal disease, and 2 patients died shortly after treatment. Microscopic examination showed inflammatory cells within the glomeruli, and immunohistochemical study revealed abundant intrarenal T cells and macrophages in CrGN cases. Strong expression of OPN was observed in tubular epithelial cells and intraglomerular macrophages. Conclusion: Cellular immune responses play a crucial role in glomerular crescents in renal amyloidosis. Immunosuppressive treatment is often ineffective and raises the risk of complications in CrGN with abundant glomerular sclerosis and tubulointerstitial injury.
AB - Background: Several studies examined glomerular crescents associated with renal amyloidosis. However, the incidence of crescents, the association between the 2 lesions, treatment and outcome are still controversial. Patients and methods: We studied 107 consecutive biopsies of renal amyloidosis, and found cellular or fibrocellular crescents in 13 cases (12.1%). We investigated the clinical characteristics, pathological findings, treatment and outcome. We also performed immunohistochemical staining using T cell, macrophage and osteopontin (OPN) markers. Results: Amyloid was of the AA type in 12 cases, and all patients had rheumatoid arthritis. Six cases with AA amyloidosis had crescentic glomerulonephritis (CrGN), and 5 presented with rapidly progressive glomerulonephritis (RPGN). The percentage of crescents correlated negatively with serum albumin (r = -0.83, p < 0.001), and positively with serum creatinine (r = 0.72, p < 0.01) and urinary protein excretion (r = 0.85, p < 0.001). All RPGN patients developed end-stage renal disease, and 2 patients died shortly after treatment. Microscopic examination showed inflammatory cells within the glomeruli, and immunohistochemical study revealed abundant intrarenal T cells and macrophages in CrGN cases. Strong expression of OPN was observed in tubular epithelial cells and intraglomerular macrophages. Conclusion: Cellular immune responses play a crucial role in glomerular crescents in renal amyloidosis. Immunosuppressive treatment is often ineffective and raises the risk of complications in CrGN with abundant glomerular sclerosis and tubulointerstitial injury.
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U2 - 10.5414/cnp70464
DO - 10.5414/cnp70464
M3 - Article
C2 - 19049702
AN - SCOPUS:57349156204
VL - 70
SP - 464
EP - 474
JO - Clinical Nephrology
JF - Clinical Nephrology
SN - 0301-0430
IS - 6
ER -