---
title: "GDF15 mediates renal adaptation to primary aldosteronism and limits hypokalemia"
id: "biorxiv-2-renal-adaptation-to-primary-aldosteronism-requires-gdf15-to-control-plasma"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-2-renal-adaptation-to-primary-aldosteronism-requires-gdf15-to-control-plasma"
content_type: "clinical_feed_article"
specialty: "Nephrology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.18.759915v1?rss=1"
published_at: "2026-10-22T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# GDF15 mediates renal adaptation to primary aldosteronism and limits hypokalemia
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-2-renal-adaptation-to-primary-aldosteronism-requires-gdf15-to-control-plasma
- **Specialty:** [Nephrology](https://medichelpline.com/clinical-feed/nephrology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.18.759915v1?rss=1)
- **Published At:** 2026-10-22T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- The study measured urinary and plasma **GDF15** in 81 patients with **primary aldosteronism** and 41 control subjects, finding a roughly threefold rise in urinary GDF15 and a 1.6-fold increase in plasma GDF15 in PA. Treatment normalized both urine and plasma levels. - Urinary GDF15 correlated with urinary aldosterone (rho=0.35, p<0.01), age, and BMI; the cohort did not show a correlation between urinary GDF15 and plasma potassium. - A murine chronic mineralocorticoid excess model (DOCP administration) produced hypokalemia in wild-type mice; the preprint reports plasma K 3.5±0.1 mM in DOCP-treated WT versus 4.3±0.1 mM in controls (p<0.01). - In **GDF15** knockout (GDF15KO) mice, DOCP-induced hypokalemia was more severe than in WT mice, indicating a protective physiological role for **GDF15** in preserving plasma potassium during mineralocorticoid excess. - DOCP increased 24-hour urinary **GDF15** twofold and upregulated GDF15 expression in the collecting duct of WT mice; GDF15KO animals lacked the collecting-duct increase and did not show the ICA proliferation seen in WT. - Single-cell or bulk transcriptomic analysis (described as producing inverted transcriptional responses in intercalated cell type A (ICA) and principal cell (PC) compartments according to genotype) suggested genotype-dependent differences in cellular response to chronic mineralocorticoid exposure. - Authors propose that **GDF15** promotes ICA proliferation, which could increase K reabsorption in the **collecting duct** and mitigate aldosterone-driven potassium loss. - The report is a preprint not peer-reviewed. The source did not report DOCP dosing or other experimental protocol specifics in the abstract; full methods are in the preprint but were not reproduced in this brief. Remaining questions include mechanism details linking transcriptomic changes to transport function and whether GDF15 alterations predict hypokalemia risk in diverse PA subgroups.
## Clinical Analysis & Structured Key Points
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Justine Billiet, Luciana Morla, Emmanuelle Vidal-Petiot, Emmanuel Wirth, Maude Laney, Stephanie Baron, Laurence Amar, Lydie Cheval, [ View ORCID Profile](http://orcid.org/0000-0001-7065-9124)Gilles Crambert doi: https://doi.org/10.64898/2026.10.18.759915 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. Justine Billiet 1 INSERM; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Justine%2BBilliet%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Billiet%20J&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJustine%2BBilliet%2B) Luciana Morla 1 INSERM; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Luciana%2BMorla%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Morla%20L&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ALuciana%2BMorla%2B) Emmanuelle Vidal-Petiot 2 APHP; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Emmanuelle%2BVidal-Petiot%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Vidal-Petiot%20E&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AEmmanuelle%2BVidal-Petiot%2B) Emmanuel Wirth 1 INSERM; 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Paradoxically, only 9 to 37% of PA patients develop hypokalemia, suggesting adaptive mechanisms. Growth differentiation factor 15 (GDF15) promotes intercalated cell type A (ICA) proliferation and K reabsorption in the collecting duct, but its role in PA is unexplored. Methods We measured urinary and plasma GDF15 in 81 PA patients (two centers) and 41 controls. A murine model of chronic mineralocorticoid excess (DOCP treatment) was used in wild-type (WT) and GDF15 knockout (GDF15KO) mice to assess renal adaptation. Results PA patients exhibited 3-fold higher urinary GDF15 and 1.6-fold higher plasma GDF15 than controls, with normalization post-treatment. 24-hour urinary GDF15 correlated with urinary aldosterone (rho=0.35, p The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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Justine Billiet, Luciana Morla, Emmanuelle Vidal-Petiot, Emmanuel Wirth, Maude Laney, Stephanie Baron, Laurence Amar, Lydie Cheval, Gilles Crambert bioRxiv 2026.10.18.759915; doi: https://doi.org/10.64898/2026.10.18.759915 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. Share This Article: Copy [![Twitter logo](https://www.biorxiv.org/sites/all/modules/highwire/highwire/images/twitter.png)](https://www.biorxiv.org/highwire_log/share/twitter?link=http%3A%2F%2Ftwitter.com%2Fshare%3Furl%3Dhttps%253A%2F%2Fwww.biorxiv.org%2Fcontent%2F10.64898%2F2026.10.18.759915v1%26text%3DRenal%2520adaptation%2520to%2520primary%2520aldosteronism%2520requires%2520GDF15%2520to%2520control%2520plasma%2520potassium%2520level%2520in%2520mice%2520and%2520human. 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