The University of Southampton
University of Southampton Institutional Repository

Clonal myelopoiesis promotes adverse outcomes in chronic kidney disease

Clonal myelopoiesis promotes adverse outcomes in chronic kidney disease
Clonal myelopoiesis promotes adverse outcomes in chronic kidney disease

We sought to determine the relationship between age-related clonal hematopoiesis (CH) and chronic kidney disease (CKD). CH, defined as mosaic chromosome abnormalities (mCA) and/or driver mutations was identified in 5449 (2.9%) eligible UK Biobank participants (n = 190,487 median age = 58 years). CH was negatively associated with glomerular filtration rate estimated from cystatin-C (eGFR.cys; β = −0.75, P = 2.37 × 10 –4), but not with eGFR estimated from creatinine, and was specifically associated with CKD defined by eGFR.cys < 60 (OR = 1.02, P = 8.44 × 10 –8). In participants without prevalent myeloid neoplasms, eGFR.cys was associated with myeloid mCA (n = 148, β = −3.36, P = 0.01) and somatic driver mutations (n = 3241, β = −1.08, P = 6.25 × 10 –5) associated with myeloid neoplasia (myeloid CH), specifically mutations in CBL, TET2, JAK2, PPM1D and GNB1 but not DNMT3A or ASXL1. In participants with no history of cardiovascular disease or myeloid neoplasms, myeloid CH increased the risk of adverse outcomes in CKD (HR = 1.6, P = 0.002) compared to those without myeloid CH. Mendelian randomisation analysis provided suggestive evidence for a causal relationship between CH and CKD (P = 0.03). We conclude that CH, and specifically myeloid CH, is associated with CKD defined by eGFR.cys. Myeloid CH promotes adverse outcomes in CKD, highlighting the importance of the interaction between intrinsic and extrinsic factors to define the health risk associated with CH.

0887-6924
507-515
Dawoud, Ahmed A Z.
01e458e9-68ea-45c1-9e8b-ef85e9ccc35e
Gilbert, Rodney D.
c69c5b99-2a15-4502-acd8-36b254d42601
Tapper, William J.
9d5ddc92-a8dd-4c78-ac67-c5867b62724c
Cross, Nicholas C. P.
f87650da-b908-4a34-b31b-d62c5f186fe4
Dawoud, Ahmed A Z.
01e458e9-68ea-45c1-9e8b-ef85e9ccc35e
Gilbert, Rodney D.
c69c5b99-2a15-4502-acd8-36b254d42601
Tapper, William J.
9d5ddc92-a8dd-4c78-ac67-c5867b62724c
Cross, Nicholas C. P.
f87650da-b908-4a34-b31b-d62c5f186fe4

Dawoud, Ahmed A Z., Gilbert, Rodney D., Tapper, William J. and Cross, Nicholas C. P. (2022) Clonal myelopoiesis promotes adverse outcomes in chronic kidney disease. Leukemia, 36 (2), 507-515. (doi:10.1038/s41375-021-01382-3).

Record type: Article

Abstract

We sought to determine the relationship between age-related clonal hematopoiesis (CH) and chronic kidney disease (CKD). CH, defined as mosaic chromosome abnormalities (mCA) and/or driver mutations was identified in 5449 (2.9%) eligible UK Biobank participants (n = 190,487 median age = 58 years). CH was negatively associated with glomerular filtration rate estimated from cystatin-C (eGFR.cys; β = −0.75, P = 2.37 × 10 –4), but not with eGFR estimated from creatinine, and was specifically associated with CKD defined by eGFR.cys < 60 (OR = 1.02, P = 8.44 × 10 –8). In participants without prevalent myeloid neoplasms, eGFR.cys was associated with myeloid mCA (n = 148, β = −3.36, P = 0.01) and somatic driver mutations (n = 3241, β = −1.08, P = 6.25 × 10 –5) associated with myeloid neoplasia (myeloid CH), specifically mutations in CBL, TET2, JAK2, PPM1D and GNB1 but not DNMT3A or ASXL1. In participants with no history of cardiovascular disease or myeloid neoplasms, myeloid CH increased the risk of adverse outcomes in CKD (HR = 1.6, P = 0.002) compared to those without myeloid CH. Mendelian randomisation analysis provided suggestive evidence for a causal relationship between CH and CKD (P = 0.03). We conclude that CH, and specifically myeloid CH, is associated with CKD defined by eGFR.cys. Myeloid CH promotes adverse outcomes in CKD, highlighting the importance of the interaction between intrinsic and extrinsic factors to define the health risk associated with CH.

Text
Dawoud Leukemia 2021 - Accepted Manuscript
Available under License Creative Commons Attribution.
Download (1MB)
Text
s41375-021-01382-3 - Version of Record
Available under License Creative Commons Attribution.
Download (1MB)

More information

Accepted/In Press date: 2 August 2021
Published date: 1 February 2022
Additional Information: Funding Information: AAZD was supported by a Lady Tata International Award; NCPC and WJT were supported by Blood Cancer UK. The authors acknowledge the use of the IRIDIS High Performance Computing Facility and associated support services at the University of Southampton.

Identifiers

Local EPrints ID: 450711
URI: http://eprints.soton.ac.uk/id/eprint/450711
ISSN: 0887-6924
PURE UUID: 5fc3b485-f52e-46d7-86bf-3de59d07abf6
ORCID for Ahmed A Z. Dawoud: ORCID iD orcid.org/0000-0003-0164-7773
ORCID for Rodney D. Gilbert: ORCID iD orcid.org/0000-0001-7426-0188
ORCID for William J. Tapper: ORCID iD orcid.org/0000-0002-5896-1889
ORCID for Nicholas C. P. Cross: ORCID iD orcid.org/0000-0001-5481-2555

Catalogue record

Date deposited: 09 Aug 2021 16:30
Last modified: 06 Nov 2024 05:01

Export record

Altmetrics

Contributors

Author: Ahmed A Z. Dawoud ORCID iD
Author: Rodney D. Gilbert ORCID iD

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×