Throughout his academic career, Thomas Verissimo has specialised in kidney diseases, with a particular focus on those linked to alterations in renal metabolism, such as chronic kidney disease (CKD). He obtained his PhD from the University of Montreal, where he investigated the pathophysiological mechanisms underlying renal carcinoma.

In 2019, he joined the Laboratory of Nephrology and Hypertension, led by Professor Sophie de Seigneux, to undertake a postdoctoral fellowship focused on CKD progression. His research centres on the role of renal tubular metabolism in the development of fibrosis and the decline of kidney function, with particular emphasis on the enzyme phosphoenolpyruvate carboxykinase 1 (PCK1). He currently holds the position of Scientific Collaborator.

RESEARCH AIMS

Dr Verissimo’s research aims to improve the understanding of renal metabolism in the progression of chronic kidney disease (CKD), a condition affecting approximately 10% of the global population and a major contributor to cardiovascular morbidity and mortality.

His work focuses specifically on metabolic alterations in the kidney, particularly the role of the enzyme PCK1. His studies have shown that dysregulation of PCK1 contributes to mitochondrial dysfunction, metabolic reprogramming, and the activation of pro-fibrotic pathways in renal tubular cells, central mechanisms in CKD progression.

By investigating the role of PCK1 and other key metabolic regulators, he seeks to identify novel therapeutic targets. The ultimate goal of this research is to develop innovative treatments that modulate renal metabolism to slow or prevent CKD progression.

EXPERTISE

• Renal metabolism

• Gluconeogenesis

• Acute and chronic kidney failure

KEY PUBLICATIONS

1.     Verissimo T, de Seigneux S. New evidence of the impact of mitochondria on kidney health and disease. Nat Rev Nephrol. 2024 Feb;20(2):81–82. doi: 10.1038/s41581‑023‑00803‑z https://www.nature.com/articles/s41581-023-00803-z

2.     Verissimo T, Faivre A, Rinaldi A, et al. Decreased renal gluconeogenesis is a hallmark of chronic kidney disease. J Am Soc Nephrol. 2022 Apr;33(4):810–827. doi: 10.1681/ASN.2021050680 https://journals.lww.com/jasn/abstract/2022/04000/decreased_renal_gluconeogenesis_is_a_hallmark_of.15.aspx

3.     Verissimo T, Dalga D, Arnoux G, et al. PCK1 is a key regulator of metabolic and mitochondrial functions in renal tubular cells. Am J Physiol Renal Physiol. 2023 Apr 27;324(6):F532–F543. doi: 10.1152/ajprenal.00038.2023 https://journals.physiology.org/doi/full/10.1152/ajprenal.00038.2023

4.     Legouis D, Ricksten SE, Faivre A, et al. Altered proximal tubular cell glucose metabolism during acute kidney injury is associated with mortality. Nat Metab. 2020 Aug;2(8):732–743. doi: 10.1038/s42255‑020‑0238‑1 https://www.nature.com/articles/s42255-020-0238-1

5.     Faivre A, et al. Tubular cell glucose metabolism shift during acute and chronic injuries. Front Med (Lausanne). 2021 Nov 5;8:742072. doi: 10.3389/fmed.2021.742072 https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2021.742072/full