Chronic Renal Failure Treatment Duration and Mode: Their Relevance to the Late Dialysis Periarticular Syndrome

Charra, Bernard; Calemard, E; Laurent, Guillaume

doi:10.1159/000169493

Cited by 71 publications

(33 citation statements)

References 4 publications

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“…In summary, β 2 -microglobulin amyloidosis is a concerning disease because of its disabling characteristics and its high incidence with increasing age and time of dialysis treatment [163, 164]. The pathogenesis of β 2 -microglobulin amyloidosis is likely to be multifactorial.…”

Section: Cellular Participation: Role Of the Macrophagesmentioning

confidence: 99%

Antiproteases and Cells in the Pathogenesis of β2-Microglobulin Amyloidosis: Role of α2-Macroglobulin and Macrophages

Argilés¹,

Mourad²,

Gouin-Charnet³

et al. 2000

Nephron

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Section: Cellular Participation: Role Of the Macrophagesmentioning

confidence: 99%

Antiproteases and Cells in the Pathogenesis of β2-Microglobulin Amyloidosis: Role of α2-Macroglobulin and Macrophages

Argilés¹,

Mourad²,

Gouin-Charnet³

et al. 2000

Nephron

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“…Dialysis-related amyloidosis (DRA) causes many musculoskeletal problems in long-term hemodialysis (HD) patients [1][2][3]. It has been reported that deposition of ß 2 -Analysis of ß 2 -Microglobulin Kinetics in Hemodialysis Blood Purif 2001;19:388-394 389 microglobulin (BMG) is associated with the occurrence of DRA [4,5].…”

Section: Introductionmentioning

confidence: 99%

Analysis of β2-Microglobulin Kinetics in Hemodialysis by a Modified Variable-Volume One-Compartment Model

Yamada¹,

Akiba

Sasaki

2001

Blood Purif

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It has been reported that deposition of β₂-microglobulin (BMG) is associated with the occurrence of dialysis-related amyloidosis (DRA) in long-term hemodialysis (HD) patients. Though reduction of the BMG burden is essential in preventing DRA, simple BMG kinetic models applicable to clinical practice have not been established. We have reported a modified variable-volume one-compartment model (1CM) for analyzing urea nitrogen (UN) kinetics, in which no specific parameters other than a modification factor are necessary. If there is a constant relation between the BMG concentration of the dialyzer arterial line and the mean BMG concentration in the body during HD, the modified 1CM may also be applied to BMG. As such, in order to verify its validity, we analyzed UN and BMG kinetics by the modified 1CM in 28 HD patients in whom polysulfone dialyzers were used, and compared the calculated and measured solute rebound. In 3 of the patients, the spent dialysate was collected in a tank, and the BMG removal mass, calculated by the modified 1CM, was compared with that recovered in the tank. The BMG rebound ratio (%), calculated by the modified 1CM, was not different from the measured one (36.3 ± 9.9 vs. 36.5 ± 11.5, p = 0.954), as in the case of UN (15.8 ± 4.5 vs. 16.3 ± 4.6, p = 0.541). The solute dilution in the blood circuit by solute disequilibrium and blood recirculations for BMG was estimated to be 74% stronger than that for UN. The normalized solute generation rate (mg/min/l) and the time-averaged solute concentration over a 1-week period (mg/l) were 0.142 ± 0.023 and 448 ± 68 for UN and 0.00578 ± 0.00125 and 22.4 ± 4.6 for BMG, respectively. The differences between these two solutes resulted in a Dilution index for BMG that was 23% lower than that for UN (2.62 ± 0.44 vs. 3.21 ± 0.39, p < 0.0001). The modified 1CM overestimated the BMG removal mass (mg) by about 20% compared with that recovered in the tank (195 ± 22 vs. 162 ± 17, p < 0.0001). One of the causes of this discrepancy was speculated to be adsorption of BMG by polysulfone dialyzers. It was concluded that, despite several problems in quantitative analysis, the modified 1CM would be a useful model for estimating the dialysis efficiency for BMG removal in clinical practice.

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“…The desig nation 'AB-amyloidosis' is derived from the precursor protein of this type of amyloidosis, which has been shown to be P2-microglobulin [1,2], the light chain of the HLA class I com plex. The prevalence of AB-amyloid deposi tion in patients on treatment for more than 10 years is estimated to range from 30 to 100% [3][4][5], Except for rare cases, the amy loidosis will not manifest clinically before 5-7 years of chronic dialysis therapy [3][4][5], The amyloidosis may affect not only pa tients on long-term hemodialysis, but also those exclusively treated with long-term he mofiltration or continuous ambulatory peri toneal dialysis [6,7], Clinical manifestations of AB-amyloid deposition are largely restricted to articular and periarticular sites [3][4][5] (table 1) and show similarities to a rare clinical manifesta tion of the immunoglobulin light chain amy loidosis (AL-amyloidosis), which is known as 'pseudorheumatoid arthritis'.…”

Section: Introductionmentioning

confidence: 99%

“…In contrast to the preferential localization of AB-amyloid deposits within structures re lated to the musculoskeletal system, other systemic manifestations, especially with re gard to organs, seem to be exceptional [3][4][5][8][9][10], The reasons underlying this preferen tial localization remain hypothetical, al though a pathogenetic role of calcium [11], glycosaminoglvcan alterations [12], iron [13], renal osteodystrophy [2] or the colla gen-binding affinity for py-microglobulin [ 14] has been proposed.…”

Section: Introductionmentioning

confidence: 99%

“…In view of the clinical manifestations, the diagnosis of AB-amyloidosis mainly has been based on the presence of the carpal tun nel syndrome and/or juxta-articular radiolucent cystic bone lesions in long-term dialysis patients [3][4][5]10], However, neither these two most common findings nor any of the other clinical manifestations of AB-amyloid osis can be regarded as pathognomonic for this disease. Consequently, the clinical or radiological diagnosis of AB-amyloidosis needs to be confirmed by more specific tests.…”

Section: Introductionmentioning

confidence: 99%

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Diagnostic Approaches to AB-Amyloidosis

Floege

1991

Blood Purif

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AB-amyloidosis, characterized by the presence of β2-microglobulin in the amyloid fibrils, has become an important complication of long-term renal replacement therapy. Due to the mainly musculoskeletal manifestation of the disease, standard approaches to obtain the diagnosis of amyloidosis, such as rectal biopsy or fat aspiration, often yield negative results. Currently, definitive diagnosis relies on biopsies, usually of synovial membranes or bone cystic radiolucencies. The serum level of β2-microglobulin, though markedly elevated, does not distinguish between patients with and without amyloid deposition. Measurements of altered, circulating β₂-microglobulin species have not yet been evaluated in this regard. Recently, two radiopharmaceuticals, namely radiolabelled serum amyloid P component and radiolabelled β2-microglobulin, have been shown to be able to detect amyloid deposits in vivo in a noninvasive manner. At least in the case of labelled β2-microglobulin it enables the specific detection of clinically and radiologically unrecognizable AB-amyloid deposits. These tests therefore may have the potential to alleviate the need for biopsy confirmation in the diagnostic workup of a suspected AB-amyloidosis.

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Chronic Renal Failure Treatment Duration and Mode: Their Relevance to the Late Dialysis Periarticular Syndrome

Cited by 71 publications

References 4 publications

Antiproteases and Cells in the Pathogenesis of β<sub>2</sub>-Microglobulin Amyloidosis: Role of α<sub>2</sub>-Macroglobulin and Macrophages

Antiproteases and Cells in the Pathogenesis of β<sub>2</sub>-Microglobulin Amyloidosis: Role of α<sub>2</sub>-Macroglobulin and Macrophages

Analysis of β<sub>2</sub>-Microglobulin Kinetics in Hemodialysis by a Modified Variable-Volume One-Compartment Model

Diagnostic Approaches to AB-Amyloidosis

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