Circulating Growth Hormone-Releasing Hormone Increases After Kidney Transplantation and Shows Divergent Associations with Gut-Derived Uremic Toxins.

Authors

Camillo Tancredi Strizzi, Leah Hernandez, Samsul Arefin, Vincenzo Cantaluppi, Francesco Pesce, Peter Stenvinkel, Karolina Kublickiene

Published in

European journal of internal medicine. Pages 107178. Sep 11, 2026. Epub Sep 11, 2026.

Abstract

The growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis is disrupted in chronic kidney disease (CKD), yet its upstream regulator, growth hormone-releasing hormone (GHRH), has never been measured in kidney failure. GHRH receptors are expressed in the kidney, and preclinical studies suggest GHRH agonists exert reno- and vasoprotective effects independent of GH. Whether GHRH changes after kidney transplantation (KTx) or relates to gut-derived uremic toxins is unknown.
Sixty patients with kidney failure were evaluated pre-transplant and at two-year follow-up. GHRH immunoreactivity (GHRH-IR) was measured by competitive ELISA alongside gut-derived uremic toxins p-cresyl sulfate (pCS), phenyl sulfate (PhS), trimethylamine-N-oxide (TMAO), and metabolic, cardiovascular and inflammatory biomarkers. pCS, PhS and TMAO were prespecified primary exposures (Benjamini-Hochberg FDR across six tests).
GHRH-IR increased by 20% after KTx (2.44 ± 0.74 to 2.93 ± 0.55 ng/mL; P < 0.0001), independently of dialysis modality and vintage. PhS inversely associated with baseline GHRH-IR (P_FDR = 0.044); the remaining pCS and PhS associations showed consistent bidirectional trends (P_FDR 0.052-0.072). Among patients with above-median baseline GHRH-IR, those with attenuated dynamics had higher TMAO than responders (112.8 vs 65.1 µM; P = 0.0006, d = 1.03). Apolipoprotein B was the strongest independent predictor of baseline GHRH-IR (β = -0.38, P = 0.002).
Circulating GHRH rises after KTx and shows differential associations with gut-derived uremic toxins. These findings, based on a relative immunoassay index, suggest a link between gut dysbiosis and somatotropic regulation in CKD.

PMID:
42728202
Bibliographic data and abstract were imported from PubMed on 12 Sep 2026.

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