NAD+ metabolism in acute kidney injury and chronic kidney disease transition

Rahil Alhumaidi; Huihui Huang; Marie Christelle Saade; Amanda J Clark; Samir M Parikh

doi:10.1016/j.molmed.2024.12.004

NAD⁺ metabolism in acute kidney injury and chronic kidney disease transition

Trends Mol Med. 2025 Jan 4:S1471-4914(24)00337-X. doi: 10.1016/j.molmed.2024.12.004. Online ahead of print.

Authors

Rahil Alhumaidi¹, Huihui Huang², Marie Christelle Saade¹, Amanda J Clark³, Samir M Parikh⁴

Affiliations

¹ Division of Nephrology, Department of Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
² Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
³ Division of Nephrology, Department of Pediatrics, University of Texas Southwestern and Children's Medical Center, Dallas, TX, USA.
⁴ Division of Nephrology, Department of Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: [email protected].

PMID: 39757045
DOI: 10.1016/j.molmed.2024.12.004

Abstract

Disturbances in kidney tubular cell metabolism are increasingly recognized as a feature of acute kidney injury (AKI). In AKI, tubular epithelial cells undergo abnormal metabolic shifts that notably disrupt NAD⁺ metabolism. Recent advancements have highlighted the critical role of NAD⁺ metabolism in AKI, revealing that acute disruptions may lead to lasting cellular changes, thereby promoting the transition to chronic kidney disease (CKD). This review explores the molecular mechanisms underlying metabolic dysfunction in AKI, with a focus on NAD⁺ metabolism, and proposes several cellular processes through which acute aberrations in NAD⁺ may contribute to long-term changes in the kidney.

Keywords: NAD(+); acute kidney injury; chronic kidney disease; fatty acid oxidation; metabolism; oxidative phosphorylation.

Publication types

Review