Lack of haemodialysis-associated amyloidosis

Zingraff, J.; Bardin, T.; Lh, Noël; Drüeke, Tilman B.

doi:10.1016/0140-6736(91)91954-s

Cited by 6 publications

(3 citation statements)

References 1 publication

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“…These methods have been criticized for not being strictly quantitative with respect to the amount and distribution of amyloid deposited (28). In addition, Gejyo (9) has recently shown that the tracer Pzm may not be deposited within the amyloid but taken up by macrophages adjacent to the amyloid deposits in bzm-derived amyloid deposits.…”

Section: Discussionmentioning

confidence: 99%

High-sensitivity diagnosis of AA amyloidosis using Congo red and immunohistochemistry detects missed amyloid deposits.

Linke

Hv²,

Michels³

1995

J Histochem Cytochem.

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Biopsy diagnosis of early amyloid-A (AA) amyloidosis has often been difficult. Examination of 57 consecutive biopsy specimens from 42 patients with inflammatory pediatric diseases permitted comparison of the precision of biopsy amyloid diagnosis in six different laboratories (labs), which applied the following methods: Congo red alone (four unspecialized labs combined as Lab 1), Congo red and electron microscopy (Lab 2), or Congo red and immunohistochemistry using monoclonal antibodies (Lab 3). Lab 3 reexamined the diagnoses made by Lab 1 and Lab 2. Of the 42 patients, 17 patients with 32 biopsies were selected for this study based on the presence of amyloid in at least one biopsy. Whereas massive or no amyloid was concordantly recognized by all labs in 18 biopsies from nine patients, discordance was demonstrated in 14 biopsies from eight patients. Comparison of Labs 1-3 revealed amyloid in 12 rectal and 18 renal biopsies evaluated by Lab 3, whereas Lab 2 missed amyloid in two of 18 renal biopsies and Lab 1 missed amyloid in 11 of 12 rectal biopsies. Most amyloid was missed when only minute amounts of amyloid were present. Had our technique (Lab 3) been available at the time of biopsy, amyloid could have been diagnosed years earlier, thereby sparing the patient further biopsies and allowing initiation of earlier treatment before organ damage could occur.

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Section: Discussionmentioning

confidence: 99%

High-sensitivity diagnosis of AA amyloidosis using Congo red and immunohistochemistry detects missed amyloid deposits.

Linke

Hv²,

Michels³

1995

J Histochem Cytochem.

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“…Renal transplantation can further halt progress of the disease [209,210], but it is controversial whether it can actually lead to regression of established Ap2M amy loid deposits [203,204,211,212], Renal transplantation also leads to rapid symptomatic improvement [209], like ly related to the usage of steroids and immunosuppressive drugs. As illustrated by the case presented, a change of the hemodialysis mode, from treatment with Cuprophane membranes to so-called 'biocompatible' hemodialyzer membranes failed to induce symptomatic relief and did not prevent further progression of the disease.…”

Section: Therapy and Prevention Of Af32m Amyloidosismentioning

confidence: 99%

“…Local deposi tion of tracer in the hip region apparently was rare. Splen ic tracer uptake in 30% of the patients was interpreted as indicating splenic amyloidosis, a notion which is not sub stantiated by histological findings [127,204], Thus, al though there is evidence that l23I-SAP can accumulate in AP2M amyloid deposits, there are at present uncertainties about both the specificity and sensitivity of this scan in hemodialysis patients. In 1990, we described our ex tended experience with 131I-p2-microglobulin scintigra phy in hemodialysis patients [81].…”

Section: Diagnosis Of A(52m Amyloidosismentioning

confidence: 99%

Beta-2-Microglobulin-Associated Amyloidosis

Floege

Ehlerding²

1996

Nephron

129

111

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β₂-Microglobulin-associated amyloidosis has emerged as a major complication of long-term renal replacement therapy. The syndrome is confined to those patients on nontransplant modes of therapy. It does not occur in patients with a functioning renal transplant or, if already present, it does not progress any further in such patients. In the population of ESRD patients on dialysis, β₂-microglobulin-associated amyloidosis affects most patients treated for more than 15 years and is a cause of significant morbidity and in rare cases even mortality. The present review, which is based on the presentation of a typical case, discusses the current knowledge on the pathogenesis, clinical manifestations, diagnosis, prevention and therapy of β_2-microblobulin-associated amyloidosis.

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Organ and Metabolic Complications: β2-Microglobulin Amyloidosis

Schaeffer

Koch

Replacement of Renal Function by Dialysis

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Lack of haemodialysis-associated amyloidosis

Cited by 6 publications

References 1 publication

High-sensitivity diagnosis of AA amyloidosis using Congo red and immunohistochemistry detects missed amyloid deposits.

High-sensitivity diagnosis of AA amyloidosis using Congo red and immunohistochemistry detects missed amyloid deposits.

Beta-2-Microglobulin-Associated Amyloidosis

Organ and Metabolic Complications: β2-Microglobulin Amyloidosis

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