Literature DB >> 15496172

Kidney and anemia in familial amyloidosis type I.

Idalina Beirão1, Luísa Lobato, Paulo M P Costa, Isabel Fonseca, Paula Mendes, Manuela Silva, Fernanda Bravo, António Cabrita, Graça Porto.   

Abstract

BACKGROUND: Familial amyloid polyneuropathy (FAP) type I is caused by a mutated transthyretin (TTR V30M) and characterized by a sensorimotor and autonomic neuropathy. Renal, cardiac, and ocular abnormalities can also occur. Anemia has been described in previous reports, but its prevalence in Portuguese FAP patients is not precisely known. The aim of this study was to estimate the prevalence of anemia in FAP type I Portuguese patients and to evaluate the contribution of erythropoietin (Epo) to its genesis.
METHODS: A retrospective cross-sectional study was undertaken to determinate the prevalence and characteristics of anemia in 165 FAP patients. For comparison analysis, 3 control groups were also evaluated, 1 group of 46 apparently healthy subjects, 1 group of 17 asymptomatic carriers of FAP-trait, and a group of 14 non-FAP patients with chronic renal insufficiency. Serum Epo levels were analyzed in all groups.
RESULTS: Anemia was present in 24.8% of symptomatic FAP patients. Iron stores, B12 vitamin, and serum folate levels were normal. FAP patients presented significantly lower serum Epo levels than healthy controls (P= 0.003). Epo levels were found lower than expected for the degree of anemia and in 17.5% were undetectable. Low Epo values were observed independently of the presence of renal failure or anemia, and sometimes preceded clinical disease.
CONCLUSION: Anemia in FAP type I is a common manifestation. The results clearly suggest a defective endogenous Epo production in the genesis of the anemia.

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Year:  2004        PMID: 15496172     DOI: 10.1111/j.1523-1755.2004.00971.x

Source DB:  PubMed          Journal:  Kidney Int        ISSN: 0085-2538            Impact factor:   10.612


  7 in total

1.  Transthyretin Val30Met mutation in an African American with cardiac amyloidosis.

Authors:  P Christian Schulze; Mathew S Maurer
Journal:  Congest Heart Fail       Date:  2010 Mar-Apr

2.  Beyond genetic factors in familial amyloidotic polyneuropathy: protein glycation and the loss of fibrinogen's chaperone activity.

Authors:  Gonçalo da Costa; Ricardo A Gomes; Ana Guerreiro; Élia Mateus; Estela Monteiro; Eduardo Barroso; Ana V Coelho; Ana Ponces Freire; Carlos Cordeiro
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3.  Transthyretin-related hereditary amyloidosis with recurrent vomiting and renal insufficiency as the initial presentation: A case report.

Authors:  Jing Xu; Meng Yang; Xiaoxia Pan; Xialian Yu; Jingyuan Xie; Hong Ren; Xiao Li; Nan Chen
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Authors:  Maria P Coutinho; Maria José Teles; Graça Melo; Marta Lopes; Delfim Duarte; Tiago L Duarte; Júlia Reis; Ana Cláudia Martins; José Carlos Oliveira; Graça Porto
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Review 5.  Guideline of transthyretin-related hereditary amyloidosis for clinicians.

Authors:  Yukio Ando; Teresa Coelho; John L Berk; Márcia Waddington Cruz; Bo-Göran Ericzon; Shu-ichi Ikeda; W David Lewis; Laura Obici; Violaine Planté-Bordeneuve; Claudio Rapezzi; Gerard Said; Fabrizio Salvi
Journal:  Orphanet J Rare Dis       Date:  2013-02-20       Impact factor: 4.123

6.  Aqueous humor erythropoietin levels in open-angle glaucoma patients with and without TTR V30M familial amyloid polyneuropathy.

Authors:  João M Beirão; Luciana M Moreira; João C Oliveira; Maria J Menéres; Bernardete B Pessoa; Maria E Matos; Paulo P Costa; Paulo A Torres; Idalina B Beirão
Journal:  Mol Vis       Date:  2014-07-02       Impact factor: 2.367

Review 7.  Diagnosis and management of transthyretin familial amyloid polyneuropathy in Japan: red-flag symptom clusters and treatment algorithm.

Authors:  Yoshiki Sekijima; Mitsuharu Ueda; Haruki Koike; Sonoko Misawa; Tomonori Ishii; Yukio Ando
Journal:  Orphanet J Rare Dis       Date:  2018-01-17       Impact factor: 4.123

  7 in total

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