University of Wisconsin–Madison Medical College of Wisconsin

Association of Rare Variants in Kidney Developmental Genes With Chronic Kidney Disease and Blood Pressure: A UK Biobank Study

Benjamin L. Spector, MD; Byunggil Yoo, MS; Neil Miller, PhD; Monica Gaddis, PhD; Isabelle Thiffault, PhD; Laurel Willig, MD

WMJ. 2025;123(1):e1-e8. Published early online March 10, 2025.

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ABSTRACT

Introduction: Chronic kidney disease (CKD) and hypertension are heritable traits. The source of this heritability remains largely unknown, and exploration has been limited principally to common genetic variants, with few studies having examined rare variants.

Methods: In this cross-sectional observational study, we evaluate whole exome sequencing data using the UK Biobank to identify the ability of rare variants in 58 kidney developmental genes to predict CKD or elevated blood pressure using logistic regression models with subgroup analysis performed by ancestry.

Results: Significant predictors of CKD included rare variants in CLCN5 (OR 1.59; 99% CI, 1.02–2.47; P = 0.007). Predictors of blood pressure included rare variants in SIX1 (OR 0.57; 99% CI, 0.35–0.94; P = 0.004) and NPHS1 (OR 0.84; 99% CI, 0.72–0.99; P = 0.005), which were protective against blood pressure elevation, and WT1 (OR 1.58; 99% CI, 1.02–2.45; P = 0.007), which was associated with elevated blood pressure. In individuals of White British ancestry, rare variants in SIX1 protected against elevated blood pressure (OR 0.58; 99% CI, 0.34–0.99; P = 0.009). Among individuals of non-White British ancestry, predictors of CKD included rare variants in SLC12A3 (OR 2.02; 99% CI, 1.08–3.78; P = 0.004) and CALB1 (OR 3.12; 99% CI, 1.15–8.47; P = 0.003). Presence of rare variants in WT1 significantly predicted elevated blood pressure (OR 2.49; 99% CI, 1.08–5.78; P = 0.005).

Conclusions: From this study, we conclude that rare variants in kidney developmental genes contribute to the risk of developing CKD and elevated blood pressure. These associations vary by ancestry.


Author Affiliations: Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin (Spector); Center for Genomic Medicine, Children’s Mercy Hospital, Kansas City, Missouri (Yoo, Thiffault, Willig); Bionano Genomics, Inc, San Diego, California (Miller); Department of Emergency Medicine, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri (Gaddis); Department of Pathology and Laboratory Medicine, Children’s Mercy Hospital, Kansas City, Missouri (Thiffault); University of Missouri-Kansas City School of Medicine, Kansas City, Missouri (Thiffault); Division of Nephrology, Children’s Mercy Hospital, Kansas City, Missouri (Willig).
Corresponding Author: Benjamin L. Spector, MD, Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, 600 Highland Ave, Madison, WI 53792; email bspector2@wisc.edu; ORCID ID 0000-0003-1800-4715
Financial Disclosures: None declared.
Funding/Support: This research was supported in part by the Children’s Mercy Hospital Clinical Research Fellowship Award, The Sam and Helen Kaplan Research Fund in Pediatric Nephrology, and The McLaughlin Family Endowed Chair in Nephrology. None of these funding entities had a role in study design; collection, analysis, or interpretation of the data; writing the report; or the decision to submit the report for publication.
Acknowledgements: This research has been conducted using the UK Biobank Resource under Application Number 65332. This work uses data provided by patients and collected by the National Health Service (NHS) as part of their care and support. We thank the Medical Writing Center at Children’s Mercy Kansas City for editing this manuscript.
Data Availability: The data generated from this study can be found within the published article and its appendices. Raw data of the UK Biobank is available from https://www.ukbiobank.ac.uk.
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