ArticleBMC nephrology2024
Non-oliguric acute renal failure secondary to a potentially lethal dose of caffeine with acute intoxication: a case report.
Article in BMC nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecently, the incidence of caffeine intoxication has been on an upward trend, with severe outcomes. However, acute kidney injury (AKI) resulting from renal pathologies secondary to caffeine intoxication is rare, and the pathophysiological mechanisms underlying AKI are unclear. CASE PRESENTATION: A female patient in her 20s ingested an over-the-counter drug containing caffeine. The patient was diagnosed with secondary non oliguric AKI caused by acute intoxication due to ingestion of a lethal dose of caffeine. On day 19 of hospitalization, a renal biopsy was performed to determine the etiology of her prolonged renal dysfunction. Light microscopy revealed normal glomeruli, mild inflammatory cell infiltration, and acute tubular damage. Myoglobin staining was positive within the tubules, with scattered myoglobin columns. Electron microscopy revealed loss of glomerular epithelial foot processes and inflated tubular mitochondria. After undergoing hemodialysis and continuous hemodiafiltration, the patient's overall condition stabilized. After a consultation with a psychiatrist, on her 34th day of hospitalization, she was discharged home.
conclusionsCaffeine 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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.