Metabolic Chaos in Kidney Disease: Unraveling Energy Dysregulation.
Level 5 - mechanism / opinion, no new human data
Narrative literature review of cellular mechanisms without new clinical data or systematic synthesis.
PubMed 39597916 · doi:10.3390/jcm13226772
What was done
The authors performed a literature review summarizing metabolic alterations in proximal tubular epithelial cells during acute kidney injury (AKI) and chronic kidney disease (CKD), alongside potential therapeutic targets identified through omics and histological techniques.
What was found
The abstract reports no quantitative data or statistical comparisons. It describes a sequence of energy dysregulation where AKI triggers a shift from fatty acid oxidation (FAO) to glycolysis to meet energy demands, which subsequently increases cellular vulnerability. In the progression from AKI to CKD, both FAO and glycolysis are downregulated, worsening cellular injury and promoting fibrosis.
Why it matters
Understanding how energy metabolism changes during kidney injury identifies specific metabolic pathways that could serve as targets to prevent the progression of acute injury to chronic renal fibrosis.
Limits
This is a narrative review presenting high-level mechanistic descriptions without original empirical data, quantitative synthesis, systematic search criteria, or clinical outcome measurements.
Cited by
- supports The primary fuel of nephrons in the renal cortex is fatty acids and ketones rather than glucose.