Non-oliguric acute renal failure secondary to a potentially lethal dose of caffeine with acute intoxication: a case report
Caffeine antagonizes adenosine receptors, stimulates ryanodine receptors, and elevates catecholamines. The onset of AKI is hypothesized to result from a combination of these mechanisms, resulting in tubular ischemia and injury, as well as renal artery constriction. The development of AKI was thought to be caused by the following factors: (1) disruption of the tubular oxygen supply-demand ratio and consequent ischemia due to adenosine receptor antagonism by caffeine, (2) tubular damage due to rhabdomyolysis and consequent ryanodine receptor stimulation, and (3) increased catecholamine levels and consequent renal artery constriction.
Authors
- Kunihiro Ishioka (ORCID: https://orcid.org/0000-0001-9129-5075)
- Takayasu Ohtake (ORCID: https://orcid.org/0000-0002-7009-161X)
- Sumi Hidaka (ORCID: https://orcid.org/0000-0002-1576-0868)
- Ayaka Mitomo (ORCID: https://orcid.org/0009-0008-3222-0960)
- Mitsuru Yanai (ORCID: https://orcid.org/0000-0001-7449-8663)
Institutions
- Shonan Kamakura General Hospital (JP)
Publication Details
- Journal
- BMC Nephrology
- Published
- 2024-12-18
- DOI
- https://doi.org/10.1186/s12882-024-03905-3
- Citations
- 2
- Primary Topic
- Muscle and Compartmental Disorders
- Type
- article
- Field-Weighted Citation Impact
- 1.15