Pathophysiology of Ketoacidosis: Core Curriculum 2026.
Level 5 - mechanism / opinion, no new human data
Narrative educational review based on mechanistic reasoning without primary empirical data.
PubMed 42340294 · doi:10.1053/j.ajkd.2026.02.646
What was done
This educational core curriculum review summarized the physiological and pathological mechanisms underlying various ketoacidotic states, including starvation ketosis, diabetic ketoacidosis, pregnancy-associated ketoacidosis, alcoholic ketoacidosis, salicylate toxicity, SGLT2 inhibitor-induced ketoacidosis, and euglycemic ketoacidosis during continuous kidney replacement therapy.
What was found
The abstract describes qualitative pathways: a reduced insulin-to-glucagon ratio and counterregulatory hormone elevation (catecholamines, cortisol, growth hormone) stimulate lipolysis and hepatic fatty acid beta-oxidation to generate acetyl-CoA and ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone). No quantitative empirical data or effect sizes are reported in the abstract.
Why it matters
It provides a unifying mechanistic framework to differentiate diverse forms of ketoacidosis, facilitating accurate clinical diagnosis and targeted intervention.
Limits
As an educational review, it presents no original patient data, lacks a systematic search or meta-analytic pooling, and reports no quantitative outcome measurements.
Cited by
- supports Fatty acid breakdown in the liver via beta-oxidation produces three ketone bodies: beta-hydroxybutyrate, acetoacetate, and acetone.