PMID: 8591057Nov 1, 1995Paper

Pathogenesis of dialysis-related amyloidosis

Current Opinion in Nephrology and Hypertension
T Miyata, K Maeda

Abstract

Beta 2-microglobulin has been demonstrated to be a major constituent of amyloid fibrils in dialysis-related amyloidosis. However, the molecular pathogenesis of this complication remains unknown. Several lines of evidence suggest that beta 2-microglobulin is not an innocent bystander, but plays an active role in the development of dialysis-related amyloidosis. The evidence remains inconclusive, however, as to whether it is intact or modified beta 2-microglobulin which is amyloidogenic and contributes to bone and joint destruction. Recent biochemical and immunohistological studies have revealed a new modification of beta 2-microglobulin in amyloid fibrils, the advanced glycation end products formed nonenzymatically between aldoses and proteins. Further study has suggested that the interaction of advanced glycation end product-modified beta 2-microglobulin with monocytes/macrophages gives a plausible, albeit incomplete, explanation for the mechanism of bone and joint destruction in dialysis-related amyloidosis. This review focuses on new aspects of the pathogenesis of dialysis-related amyloidosis.

Citations

Jun 23, 2006·Clinical and Experimental Nephrology·Hiroaki OgataSusumu Taguchi
Jan 5, 2002·The American Journal of Surgical Pathology·Sharon L MountNicholas J Hardin
Apr 1, 2000·Journal of Chromatography. B, Biomedical Sciences and Applications·V DavankovE Yousha

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