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Recent progress in understanding dialysis-related amyloidosis
Suguru Yamamoto1, Junichiro James Kazama, Ichiei Narita
1Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Science, Niigata, 951-8510, Japan.
Bone
|March 24, 2009
Summary
Dialysis-Related Amyloidosis (DRA) significantly impacts long-term dialysis patients, causing severe bone and joint issues. Understanding beta(2)-microglobulin amyloid formation is key to managing this complication alongside chronic kidney disease-mineral and bone disorder (CKD-MBD).
Area of Science:
- Nephrology
- Biochemistry
- Pathology
Background:
- Dialysis-Related Amyloidosis (DRA) is a significant complication in end-stage renal disease (ESRD) patients.
- DRA manifests as osteoarticular lesions, complicating the management of chronic kidney disease-mineral and bone disorder (CKD-MBD).
- The relationship between DRA and CKD-MBD remains debated in clinical practice.
Purpose of the Study:
- To elucidate the pathogenesis of beta(2)-microglobulin (Aβ2M) amyloid fibril formation in DRA.
- To identify factors influencing amyloid fibril stabilization and acceleration.
- To assess the clinical impact of DRA on long-term dialysis patients.
Main Methods:
- In vitro studies examining beta(2)-microglobulin amyloid fibril formation, extension, and depolymerization.
- Analysis of the role of Apoliprotein E, proteoglycans, glycosaminoglycans, lysophospholipids, and fatty acids in amyloidogenesis.
- Clinical observation of osteoarticular disorder frequency and severity correlated with dialysis duration.
Main Results:
- Beta(2)-microglobulin amyloid fibril formation, extension, and depolymerization mechanisms were clarified.
- Specific molecules (Apoliprotein E, proteoglycans, glycosaminoglycans) were identified as stabilizers of amyloid fibrils.
- Lysophospholipids and non-esterified fatty acids were found to accelerate amyloid fibril formation in vitro, potentially enhancing in vivo deposition.
- Osteoarticular disorder severity and frequency increase with dialysis duration, with significant complications observed in patients on dialysis for over 30 years.
Conclusions:
- DRA pathogenesis involves beta(2)-microglobulin amyloid fibril dynamics.
- Certain biomolecules and lipids influence amyloid deposition, impacting DRA progression.
- DRA represents a major cause of osteoarticular complications, severely affecting quality of life and daily activities in long-term dialysis patients, and is intrinsically linked to CKD-MBD management.
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