Non-oliguric acute renal failure secondary to a potentially lethal dose of caffeine with acute intoxication: a case report

Abstract

Background: Recently, 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.

Conclusions: 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.

Keywords: Acute caffeine intoxication; Acute kidney injury; Renal biopsy.

Fig. 1

Renal biopsy findings are depicted. (A) Periodic acid–Schiff histological staining does not reveal any substantial findings of the glomerulus (400x magnification). (B) Focal inflammatory cell infiltration within the interstitium, denaturation of tubular epithelium, and detachment of tubular epithelium from the basement membrane are observed on hematoxylin and eosin staining (400x magnification). (C)(D) These two images reveal the positive findings of myoglobin within the renal tubules, with the presence of myoglobin casts on myoglobin staining. (C) 200x magnification and (D) 400x magnification. (E) This image depicts the mild loss of epithelial foot processes in the glomerulus, by electron microscopy (12 00x magnification). (F) The mitochondria of the proximal tubules exhibit uniform distension, with obscure cristae, by electron microscopy (25 00x magnification)

Fig. 2

The underlying mechanisms of acute kidney injury of the present case are depicted. (1) Dehydration, cardiopulmonary arrest, and elevated levels of catecholamines have reduced the glomerular filtration rate. (2) Perturbation of the tubular oxygen demand-to-supply ratio with ensuing ischemia occurs, due to adenosine receptor antagonism. (3) Tubular impairment arises from rhabdomyolysis, consequent to ryanodine receptor stimulation