Acute Renal Injury Trigger By Confirmed Psilocybe Cubensis Mushroom Ingestion - PMC Humans have been consuming hallucinogenic mushrooms for centuries [3]. The Psilocybe cubensis mushroom is likely one of the extra generally sought species by people utilizing hallucinogenic mushrooms recreationally.

The hallucinogenic compound in Psilocybe mushrooms is the tryptamine molecule, psilocybin. As soon as ingested, psilocybin is dephosphorylated by the alkaline phosphatase enzyme to the active metabolite, psilocin [4], [5]. Each psilocin and psilocybin resemble the chemical structure of the serotonin molecule, and, not surprisingly, have affinity for a number of serotonergic receptors, together with 5-HT2A, 5HT2C, 5-HT1A, and 5-HT1D [4]. Agonism at the 5-HT2A receptor is believed to account for a lot of the hallucinatory properties of those molecules [1], [5].

Indicators and symptoms of Psilocybe mushroom ingestion embrace perceptual distortions (together with visible hallucinations), euphoria, anxiety, agitation, mydriasis, tachycardia, hypertension and flushing. Signs occur within 20-60 min of ingestion and generally resolve within 4-6 h [6], [7].

Ingestion of Psilocybe mushrooms is regarded as having a low potential for hurt. The mostly reported opposed results are unfavorable sensory experiences, where individuals present severely agitated, confused and anxious, with impaired concentration and judgment. The rare fatalities associated with Psilocybe ingestion seem associated to co-ingestion with another drug (often alcohol) or trauma [8].

Nephrotoxicity has been described following ingestion of a lot of mushrooms types, most commonly Cortinarius species, as well as some species of Amanita.

Mushrooms of the Cortinarius genus comprise the toxin orellanine [9]. Reported cases of orellanine poisoning describe a delayed onset of renal harm (~3-20 days) after mushroom ingestion. Orellanine toxin has been demonstrated in in vitro studies to cause inhibition of protein, RNA and DNA synthesis, and has also been shown to produce an ortho-semiquinone radical that can lead to oxidative stress, suggesting that the noticed renal injury occurs by means of direct toxicity to the renal tubular epithelium inflicting tubular necrosis, interstitial nephritis and fibrosis [10]. Case cohorts of exposures are reported, with a excessive proportion of patients growing irreversible renal failure requiring dialysis and even transplant [11], [12].

An “Amanita nephrotoxic syndrome” is well acknowledged following publicity to Amanita smithiana and A. proxima [12]. Though the chemical buildings of the toxins responsible haven''t been isolated, a toxin just like A. smithiana has been identified in different Amanita species including A. boudieri, A. gracilior and A. echinocephala. These patients usually current with nausea and vomiting 2-12 h after mushroom ingestion. Renal injury develops after 2-6 days, related to mild hepatitis. Renal biopsies in these cases show acute tubular necrosis and interstitial nephritis with restoration of renal perform after supportive care and often hemodialysis [12].

Other mushrooms reminiscent of A. phalloides, A. virosa, and A. bisporigera containing amatoxin produce a clinical image that is distinct from other nephrotoxic mushroom ingestions with severe gastrointestinal symptoms (nausea, vomiting, diarrhea) creating 6-24 h post ingestion, adopted by fulminant hepatotoxicity related to AKI. The renal damage is presumed secondary hepatorenal syndrome or direct renal toxicity from amatoxin [13].

There are two case stories in the literature describing doable association of “magic mushroom” ingestion and renal harm. The primary was of a 28-year-old man who introduced with renal failure and required dialysis [11]. He had mistakenly eaten a Cortinarius mushroom, as a substitute of a hallucinogenic mushroom. On renal biopsy, orellanine toxin was detected, confirming the publicity.

The second case was a 20-yr-old woman who introduced with symptomatic renal failure 5 days after ingesting what she believed to be “magic mushrooms” [14]. Her symptoms resolved with supportive therapy, and she didn''t require renal substitute therapies. Of word, she denied experiencing the anticipated hallucinations or altered sensorium after ingesting the mushrooms. The authors suspected that this affected person''s renal failure was in fact on account of consumption of a Cortinarius mushroom, nevertheless the identity of the mushroom she ate was by no means confirmed, and the patient was misplaced to observe-up.

Here, we report a case of a affected person with proof of AKI on day 2 submit-ingestion of confirmed Psilocybe cubensis mushroom. Based on the temporal association of exposure to the mushrooms within the absence of some other attainable trigger, we now have hypothesized that the AKI was associated to Psilocybe cubensis ingestion. Though renal biopsy was not performed, different options of his clinical presentation have been in step with acute tubular necrosis (ATN) including the sudden rise in creatinine, microscopic hematuria, and no leukocytes or casts in the urine. Whereas the psilocybin and psilocin molecules usually are not known to cause ATN, in principle, their affinity for serotonergic receptors could have some vasoconstricting effects that might alter renal hemodynamics, a identified risk issue for ATN [1].

We considered the chance that the spores bought on the internet were contaminated with one other nephrotoxic substance; nonetheless, the opposite people who ingested the mushrooms from the identical crop did not change into in poor health, which can be expected if there have been a toxic contaminant. One other chance is that there may have been significant intra-batch variability, and that our affected person was uncovered to a better quantity of a but-unidentified toxic contaminant or a higher quantity of psilocybin leading to increased serotonergic exercise. There may even be unidentified predisposing components that contribute to the event of ATN following Psilocybe mushroom ingestion. For instance, the case of the 20-12 months-previous female who developed AKI after the ingestion of “magic mushrooms” shares similarities to our case. Sadly, the identity of that mushroom shouldn''t be identified.

This case identifies that there could also be potential for reversible nephrotoxicity following exposure to Psilocybe mushrooms. With Buy magic mushrooms , the AKI in our patient resolved with out sequelae.