Medical Mycology Case Reports 23 (2019) 55–57

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Medical Mycology Case Reports

journal homepage: www.elsevier.com/locate/mmcr

Acute renal injury cause by confirmed Psilocybe cubensis mushroom T

ingestion
Emily Austina,b, , Hilary S. Myronc, Richard K. Summerbelld, Constance A. Mackenzieb,e
⁎

a
Emergency Medicine, University of Toronto, Toronto, Ontario, Canada
b
Ontario Poison Centre, Toronto, Ontario, Canada
c
Department of Pediatrics, University of Ottawa, Ottawa, Ontario, Canada and Montfort Hospital, Ottawa, Ontario, Canada
d
Occupational & Environmental Health, Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada and Sporometrics, Toronto, Ontario, Canada
e
Clinical Pharmacology and Toxicology/Respirology, Western University, London, Ontario, Canada and Clinical Pharmacology and Toxicology, Hospital for Sick Children,
Toronto, Ontario, Canada

ARTICLE INFO ABSTRACT

Keywords: Psilocybe mushrooms are consumed for their hallucinogenic properties. Fortunately, there are relatively few
Psilocybe adverse effects associated with their consumption. This is the first reported case of acute kidney injury (AKI)
Nephrotoxicity secondary to confirmed ingestion of Psilocybe cubensis mushroom.
Mushrooms A 15-year-old male developed symptomatic AKI 36 h post-ingestion of Psilocybe cubensis mushrooms. He was
Kidney injury
admitted to hospital with hypertension, nausea and abdominal pain and a creatinine of 450 mmol/L. A sample of
the crop of mushrooms was confirmed by mass spectrometry to contain psilocin. On day 5 post-admission, he
was discharged home. Outpatient follow-up confirmed complete resolution of his renal function.

1. Introduction 5 mmol/L (reference range 3.0–7.0 mmol/L). He was referred to a pe-

diatric tertiary care hospital, where he was admitted with further
Psilocybe mushrooms are often consumed for their hallucinogenic evaluation by the nephrology team. On the day of admission (day zero)
properties. Despite the apparent popularity of these mushrooms, rela- he was hypertensive with a blood pressure of 144/85. Admission
tively few adverse effects are have been reported from their use, with bloodwork included a CBC, LFTs, electrolytes, calcium panel, blood
most being benign and self-limited [1]. Here, we report on a patient cultures and a CK. All were within the normal ranges, with the excep-
who developed symptomatic acute kidney injury (AKI) after ingesting tion of an elevated phosphate (1.98 mmol/L, reference range
Psilocybe cubenesis mushrooms. 0.90–1.50 mmol/L). Urine microscopy revealed 5–10 red blood cells
per high power field (RBC/HPF), and no protein, leukocytes, or casts. A
2. Case renal ultrasound showed normal-sized kidneys bilaterally and enhanced
cortical echogenicity. Additional investigations included normal com-
A 15-year-old male bought a “grow kit” for Psilocybe cubensis plement levels, negative antistreptolysin O titres, negative urine cul-
mushrooms from an online website. He germinated the spores into tures and two sets of negative blood cultures.
mushrooms and ate his “harvest” with three of his friends. All boys Prior to definitive identification of the ingested mushrooms, the
experienced hallucinatory effects, which resolved completely over a 6-h initial clinical presentation appeared consistent with possible ingestion
period. of an orellanine-containing mushroom. During his hospital stay, he
36 h after ingestion, the patient developed nausea, abdominal dis- received supportive care with IV fluids, hydralazine for hypertension,
comfort and low back pain. He did not experience vomiting, diarrhea, and IV N-acetyl cysteine based on case reports of benefit for orellanine-
or fevers. Initial bloodwork ordered by his primary care provider induced renal injury. On day 5 post-admission, he was discharged
showed a creatinine of 207 micromoles/L. home. Serum creatinine and phosphate levels were resolving at 108
After two days, the patient's symptoms persisted. Repeat bloodwork micromoles/L and 1.68 mmol/L respectively. Having ruled out in-
showed worsening of his renal function with a creatinine of 444 mi- fectious and rheumatologic causes, the discharge diagnosis was pre-
cromoles/L (reference range 65–121 micromoles/L) and a urea of 13. sumed AKI from mushroom ingestion.

⁎
Corresponding author at: Emergency Medicine, University of Toronto, Toronto, Ontario, Canada.
E-mail address: [email protected] (E. Austin).

https://doi.org/10.1016/j.mmcr.2018.12.007
Received 13 December 2018; Received in revised form 20 December 2018; Accepted 21 December 2018
Available online 22 December 2018
2211-7539/ © 2019 The Authors. Published by Elsevier B.V. on behalf of International Society for Human and Animal Mycology. This is an open access article
under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).
E. Austin et al. Medical Mycology Case Reports 23 (2019) 55–57

Fig. 1. Sample of crop of Psilocybe cubensis mushroom ingested by our patient.

At a 3-month follow up visit, the patient remained asymptomatic, [6,7].

with normal blood pressure and full recovery of his renal function. His Ingestion of Psilocybe mushrooms is regarded as having a low po-
creatinine was 80 micromoles/L, with a urea of 4.7 mmol/L, and tential for harm. The most commonly reported adverse effects are ne-
normal electrolytes. Urinalysis was normal. gative sensory experiences, where people present severely agitated,
A sample of the crop of mushrooms yielding the ingested specimens confused and anxious, with impaired concentration and judgment. The
(Fig. 1) was sent to a mycologist who identified the species as Psilocybe rare fatalities associated with Psilocybe ingestion seem related to co-
cubensis [2]. The identification of the mushroom sample was based on ingestion with another drug (often alcohol) or trauma [8].
shared characteristics with published descriptions of the Psilocybe cu- Nephrotoxicity has been described following ingestion of a number
bensis mushroom, including the overall stature of the basidome, the of mushrooms types, most commonly Cortinarius species, as well as
presence of a prominent annulus derived from a partial veil, a blue- some species of Amanita.
staining reaction of tissues, coloring of the pileus and the stipe, the Mushrooms of the Cortinarius genus contain the toxin orellanine [9].
concentric arrangement of the scales, and the lamellae bearing purple- Reported cases of orellanine poisoning describe a delayed onset of renal
brown basidiospores with germ pores. A sample of the mushroom crop injury (~3–20 days) after mushroom ingestion. Orellanine toxin has
was further analyzed by mass spectrometry (LC-MS/MS). Briefly, been demonstrated in in vitro studies to cause inhibition of protein,
5–10 μL of extracted mushroom (in methanol) was injected and sepa- RNA and DNA synthesis, and has also been shown to produce an ortho-
rated using a ToxTyper (Bruker) triple quadrupole liquid chromato- semiquinone radical that can lead to oxidative stress, suggesting that
graphy coupled to mass spectrometer (LC-MS/MS). The sample was the observed renal injury occurs through direct toxicity to the renal
analyzed in alternating polarity mode using the Toxtyper system tubular epithelium causing tubular necrosis, interstitial nephritis and
equipped with an electrospray ionization source. Full scan MS, MS2 and fibrosis [10]. Case cohorts of exposures are reported, with a high pro-
MS3 spectra were acquired in data dependent MS/MS mode. The Tox- portion of patients developing irreversible renal failure requiring dia-
typer system identifies compounds based on retention time, MS, MS2, lysis and even transplant [11,12].
and if necessary, MS3 information. A peak was identified with a re- An “Amanita nephrotoxic syndrome” is well recognized following
tention time of 2.5 min, corresponding to psilosin. No other peaks were exposure to Amanita smithiana and A. proxima [12]. Although the che-
identified, including for orellanine or amatoxin. mical structures of the toxins responsible have not been isolated, a toxin
The three other boys who ingested the patient's ‘crop’ at the same similar to A. smithiana has been identified in other Amanita species
time also presented to their physicians for evaluation on the advice of including A. boudieri, A. gracilior and A. echinocephala. These patients
the medical team. They all remained asymptomatic and had normal typically present with nausea and vomiting 2–12 h after mushroom
renal function. ingestion. Renal injury develops after 2–6 days, associated with mild
hepatitis. Renal biopsies in these cases demonstrate acute tubular ne-
3. Discussion crosis and interstitial nephritis with recovery of renal function after
supportive care and occasionally hemodialysis [12].
Humans have been consuming hallucinogenic mushrooms for cen- Other mushrooms such as A. phalloides, A. virosa, and A. bisporigera
turies [3]. The Psilocybe cubensis mushroom is one of the more com- containing amatoxin produce a clinical picture that is distinct from
monly sought species by people using hallucinogenic mushrooms re- other nephrotoxic mushroom ingestions with severe gastrointestinal
creationally. symptoms (nausea, vomiting, diarrhea) developing 6–24 h post inges-
The hallucinogenic compound in Psilocybe mushrooms is the tryp- tion, followed by fulminant hepatotoxicity associated with AKI. The
tamine molecule, psilocybin. Once ingested, psilocybin is depho- renal injury is presumed secondary hepatorenal syndrome or direct
sphorylated by the alkaline phosphatase enzyme to the active meta- renal toxicity from amatoxin [13].
bolite, psilocin [4,5]. Both psilocin and psilocybin resemble the There are two case reports in the literature describing possible as-
chemical structure of the serotonin molecule, and, not surprisingly, sociation of “magic mushroom” ingestion and renal injury. The first was
have affinity for several serotonergic receptors, including 5-HT2A, of a 28-year-old man who presented with renal failure and required
5HT2C, 5-HT1A, and 5-HT1D [4]. Agonism at the 5-HT2A receptor is dialysis [11]. He had mistakenly eaten a Cortinarius mushroom, instead
believed to account for most of the hallucinatory properties of these of a hallucinogenic mushroom. On renal biopsy, orellanine toxin was
molecules [1,5]. detected, confirming the exposure.
Signs and symptoms of Psilocybe mushroom ingestion include per- The second case was a 20-year-old woman who presented with
ceptual distortions (including visual hallucinations), euphoria, anxiety, symptomatic renal failure 5 days after ingesting what she believed to be
agitation, mydriasis, tachycardia, hypertension and flushing. Symptoms “magic mushrooms” [14]. Her symptoms resolved with supportive
occur within 20–60 min of ingestion and generally resolve within 4–6 h treatment, and she did not require renal replacement therapies. Of note,

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E. Austin et al. Medical Mycology Case Reports 23 (2019) 55–57

she denied experiencing the expected hallucinations or altered sen- from the Hospital of Sick Children, who assisted us with the mass
sorium after ingesting the mushrooms. The authors suspected that this spectrometry analysis of the crop specimen.
patient's renal failure was in fact due to consumption of a Cortinarius
mushroom, however the identity of the mushroom she ate was never Conflict of interest
confirmed, and the patient was lost to follow-up.
Here, we report a case of a patient with evidence of AKI on day 2 There are none.
post-ingestion of confirmed Psilocybe cubensis mushroom. Based on the
temporal association of exposure to the mushrooms in the absence of References
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Acknowledgements

We gratefully acknowledge the contribution of Dr. David Colantonio

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