Glomerular expression of matrix metalloproteinases in AL-amyloidosis and association with renal function at the time of kidney biopsy

Evangelia Charitaki, Efstathios Kastritis, Constantina Petraki, Konstantinos Liapis, Konstantinos Adamidis, Theophanis Apostolou, Christallenia Christodoulidou, Nikoleta Nikolopoulou, Evangelos Terpos, Lydia Nakopoulou, Meletios A Dimopoulos
Clinical Nephrology 2016, 85 (1): 44-54

BACKGROUND: Matrix metalloproteinases (MMPs) have been implicated in the pathophysiology of various renal diseases, however, there are limited data regarding their role in renal AL-amyloidosis. In the present study, we evaluated the glomerular expression of MMPs in renal-biopsy specimens containing AL-amyloid deposits. We also examined the association of MMPs with renal function at the time of diagnostic renal biopsy.

METHODS: We performed immunohistochemistry with monoclonal antibodies against MMP-1, MMP-2, MMP-3, MMP-9, and TIMP-1 in 19 kidney-biopsy specimens with AL-amyloidosis and 8 specimens from normal kidney tissue. We used clinical data of the patients at the time of kidney biopsy to evaluate the association between MMP expression and renal function.

RESULTS: We found increased MMP-1 and MMP-3 expression within the amyloid deposits and adjacent tissues in > 50% of the amyloid-positive biopsies, whereas MMP-1 and MMP-3 were negative in control samples. In contrast, we found no significant glomerular MMP-2 and TIMP-1 expression in amyloid-containing or normal kidneys. MMP-9 expression was found in the glomerular basement membrane equally in AL-amyloidosis and control specimens. The presence of MMP-1 and MMP-3 in the glomeruli of patients with AL-amyloidosis correlated with worse renal function at the time of kidney biopsy.

CONCLUSION: The findings of this study show increased glomerular expression of MMP-1 and MMP-3 in patients with AL-amyloidosis which is associated with worse renal function at the time of the kidney biopsy. Our results suggest an important role for MMP-1 and MMP-3 in the pathogenesis of renal damage in AL-amyloidosis.

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