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Reply to ‘Kidney involvement in hereditary transthyretin amyloidosis: is there a role for cystatin C?’

Reply to ‘Kidney involvement in hereditary transthyretin amyloidosis: is there a role for... We have read with interest the letter by Dr D'Ambriosio et al., which highlights the possible underestimation of chronic kidney disease in patients with hereditary transthyretin amyloidosis (ATTR). In a series of 19 patients with neurological or mixed phenotype of ATTR, D'Ambriosio et al. showed that the combined creatinine–cystatin C equation revealed a more altered estimated glomerular filtration rate than creatinine-based equations. This difference could be related to the decreased muscular mass of patients with symptomatic ATTR, with lower serum creatinine despite altered glomerular filtration. We are in agreement with this analysis, and we have now implemented in our centres the systematic measurement of serum cystatin C, in addition to serum creatinine, to estimate glomerular filtration rate based on the creatinine-cystatin equation. Our work has also encouraged cardiologists and neurologists to assess annually proteinuria and microalbuminuria in patients followed-up for hereditary ATTR amyloidosis. In addition to providing an effective evaluation of kidney function, this annual kidney assessment will accurately assess the kidney response to the different therapeutic strategies in hereditary ATTR. CONFLICT OF INTEREST STATEMENT None declared. © The Author(s) 2022. Published by Oxford University Press on behalf of the ERA. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical Kidney Journal Oxford University Press

Reply to ‘Kidney involvement in hereditary transthyretin amyloidosis: is there a role for cystatin C?’

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Publisher
Oxford University Press
Copyright
© The Author(s) 2022. Published by Oxford University Press on behalf of the ERA.
ISSN
2048-8505
eISSN
2048-8513
DOI
10.1093/ckj/sfac157
Publisher site
See Article on Publisher Site

Abstract

We have read with interest the letter by Dr D'Ambriosio et al., which highlights the possible underestimation of chronic kidney disease in patients with hereditary transthyretin amyloidosis (ATTR). In a series of 19 patients with neurological or mixed phenotype of ATTR, D'Ambriosio et al. showed that the combined creatinine–cystatin C equation revealed a more altered estimated glomerular filtration rate than creatinine-based equations. This difference could be related to the decreased muscular mass of patients with symptomatic ATTR, with lower serum creatinine despite altered glomerular filtration. We are in agreement with this analysis, and we have now implemented in our centres the systematic measurement of serum cystatin C, in addition to serum creatinine, to estimate glomerular filtration rate based on the creatinine-cystatin equation. Our work has also encouraged cardiologists and neurologists to assess annually proteinuria and microalbuminuria in patients followed-up for hereditary ATTR amyloidosis. In addition to providing an effective evaluation of kidney function, this annual kidney assessment will accurately assess the kidney response to the different therapeutic strategies in hereditary ATTR. CONFLICT OF INTEREST STATEMENT None declared. © The Author(s) 2022. Published by Oxford University Press on behalf of the ERA. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

Journal

Clinical Kidney JournalOxford University Press

Published: Jun 16, 2022

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