Rare Case of Acute Renal Failure Linked to Lethal Caffeine Overdose Highlights Risks of Intoxication
Japan: A recent case report published in BMC Nephrology has highlighted the severe and potentially life-threatening effects of caffeine overdose, particularly its association with acute kidney injury (AKI).
The researchers reported a case of acute kidney injury diagnosed as a result of potentially lethal caffeine intoxication. Along with the findings from a renal biopsy, multiple pathophysiological mechanisms underlying caffeine-induced AKI were considered in understanding the condition.
Energy drinks and non-drowsy medications, which are both affordable and easily accessible, have become increasingly popular. However, as the market for these products grows, there have been reported cases of suicide attempts involving the ingestion of large amounts of caffeine, some of which have been fatal. In response to rising concerns about caffeine addiction, certain countries have implemented laws to limit the amount of caffeine that can be purchased.
While caffeine intoxication has become more common, leading to various health complications, AKI caused by caffeine overdose remains rare, and the exact mechanisms behind it are not yet fully understood. Ayaka Mitomo, Kidney Disease and Transplant Center, Shonan Kamakura General Hospital, 1370-1 Okamoto, Kamakura, Kanagawa, Japan, and colleagues described the case of a female patient in her 20s who ingested an over-the-counter drug containing a lethal dose of caffeine, leading to secondary non-oliguric acute kidney injury (AKI).
Upon hospitalization, the patient was diagnosed with acute intoxication due to a caffeine overdose. On day 19, a renal biopsy was performed to investigate the cause of her prolonged renal dysfunction. Light microscopy showed normal glomeruli, mild inflammatory cell infiltration, and acute tubular damage. Myoglobin staining within the tubules revealed scattered myoglobin columns, indicating rhabdomyolysis. Electron microscopy further revealed the loss of glomerular epithelial foot processes and enlarged tubular mitochondria. The patient underwent hemodialysis and continuous hemodiafiltration, which helped stabilize her condition. Following a psychiatric consultation, she was discharged on the 34th day of hospitalization.
The researchers concluded that caffeine’s ability to antagonize adenosine receptors, stimulate ryanodine receptors, and elevate catecholamines likely contributes to the onset of acute kidney injury. The development of AKI, in this case, was hypothesized to result from a combination of factors: (1) caffeine-induced disruption of the tubular oxygen supply-demand ratio, leading to ischemia; (2) tubular damage caused by rhabdomyolysis and subsequent ryanodine receptor stimulation; and (3) renal artery constriction due to increased catecholamine levels. These mechanisms together may explain the renal dysfunction observed in caffeine intoxication.
"Caffeine is affordable and readily available without needing a doctor’s consultation or prescription. However, as demonstrated by this case, excessive caffeine intake can lead to severe renal dysfunction. Consequently, manufacturers of caffeine-based products should include prominent warnings about the potential risk of kidney injury associated with overconsumption," the researchers wrote.
Reference:
Mitomo, A., Ishioka, K., Yanai, M. et al. Non-oliguric acute renal failure secondary to a potentially lethal dose of caffeine with acute intoxication: a case report. BMC Nephrol 25, 451 (2024). https://doi.org/10.1186/s12882-024-03905-3
Disclaimer: This website is primarily for healthcare professionals. The content here does not replace medical advice and should not be used as medical, diagnostic, endorsement, treatment, or prescription advice. Medical science evolves rapidly, and we strive to keep our information current. If you find any discrepancies, please contact us at corrections@medicaldialogues.in. Read our Correction Policy here. Nothing here should be used as a substitute for medical advice, diagnosis, or treatment. We do not endorse any healthcare advice that contradicts a physician's guidance. Use of this site is subject to our Terms of Use, Privacy Policy, and Advertisement Policy. For more details, read our Full Disclaimer here.
NOTE: Join us in combating medical misinformation. If you encounter a questionable health, medical, or medical education claim, email us at factcheck@medicaldialogues.in for evaluation.