Acute Renal Injury Cause By Confirmed Psilocybe Cubensis Mushroom Ingestion

Humans have been consuming hallucinogenic mushrooms for centuries [3]. The Psilocybe cubensis mushroom is without doubt one of the extra generally sought species by folks using 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 lively metabolite, psilocin [4], [5]. Where to buy magic mushrooms and psilocybin resemble the chemical structure of the serotonin molecule, and, not surprisingly, have affinity for several serotonergic receptors, including 5-HT2A, 5HT2C, 5-HT1A, and 5-HT1D [4]. Agonism at the 5-HT2A receptor is believed to account for most of the hallucinatory properties of these molecules [1], [5].

Indicators and signs of Psilocybe mushroom ingestion include perceptual distortions (together with visual hallucinations), euphoria, anxiety, agitation, mydriasis, tachycardia, hypertension and flushing. Symptoms happen within 20-60 min of ingestion and generally resolve inside 4-6 h [6], [7].

Ingestion of Psilocybe mushrooms is regarded as having a low potential for harm. The mostly reported adversarial results are unfavourable sensory experiences, where individuals current severely agitated, confused and anxious, with impaired concentration and judgment. The uncommon fatalities related to Psilocybe ingestion appear associated to co-ingestion with another drug (usually alcohol) or trauma [8].

Nephrotoxicity has been described following ingestion of quite a few mushrooms sorts, mostly Cortinarius species, in addition to some species of Amanita.

Mushrooms of the Cortinarius genus include the toxin orellanine [9]. Reported cases of orellanine poisoning describe a delayed onset of renal injury (~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 proven to provide an ortho-semiquinone radical that may lead to oxidative stress, suggesting that the observed renal damage happens via direct toxicity to the renal tubular epithelium inflicting tubular necrosis, interstitial nephritis and fibrosis [10]. Case cohorts of exposures are reported, with a high proportion of patients developing irreversible renal failure requiring dialysis and even transplant [11], [12].

An “Amanita nephrotoxic syndrome” is nicely recognized following exposure to Amanita smithiana and A. proxima [12]. Although the chemical buildings of the toxins accountable haven't been isolated, a toxin just like A. smithiana has been recognized in other 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 harm develops after 2-6 days, associated with mild hepatitis. Renal biopsies in these instances exhibit acute tubular necrosis and interstitial nephritis with recovery of renal function after supportive care and sometimes hemodialysis [12].

Different mushrooms resembling A. phalloides, A. virosa, and A. bisporigera containing amatoxin produce a clinical picture that is distinct from different nephrotoxic mushroom ingestions with severe gastrointestinal signs (nausea, vomiting, diarrhea) growing 6-24 h publish ingestion, followed 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 reports in the literature describing attainable association of “magic mushroom” ingestion and renal damage. The first was of a 28-yr-outdated man who offered with renal failure and required dialysis [11]. He had mistakenly eaten a Cortinarius mushroom, as an alternative of a hallucinogenic mushroom. On renal biopsy, orellanine toxin was detected, confirming the exposure.

The second case was a 20-year-outdated woman who offered with symptomatic renal failure 5 days after ingesting what she believed to be “magic mushrooms” [14]. Her symptoms resolved with supportive treatment, and she didn't require renal replacement therapies. Of be aware, she denied experiencing the expected hallucinations or altered sensorium after ingesting the mushrooms. The authors suspected that this affected person's renal failure was in actual fact attributable to consumption of a Cortinarius mushroom, nonetheless the identity of the mushroom she ate was never confirmed, and the affected person was lost to comply with-up.

Right here, we report a case of a patient with proof of AKI on day 2 put up-ingestion of confirmed Psilocybe cubensis mushroom. Based on the temporal affiliation of publicity to the mushrooms within the absence of any other attainable cause, now we have hypothesized that the AKI was associated to Psilocybe cubensis ingestion. Although renal biopsy was not done, different features of his clinical presentation have been per acute tubular necrosis (ATN) including the sudden rise in creatinine, microscopic hematuria, and no leukocytes or casts within the urine. Whereas the psilocybin and psilocin molecules are not known to trigger ATN, in idea, their affinity for serotonergic receptors might have some vasoconstricting effects that might alter renal hemodynamics, a known threat factor for ATN [1].

We thought of the likelihood that the spores bought on the internet had been contaminated with another nephrotoxic substance; nevertheless, the opposite individuals who ingested the mushrooms from the same crop didn't turn into sick, which could be expected if there were a toxic contaminant. One other chance is that there may have been important intra-batch variability, and that our affected person was exposed to a larger amount of a yet-unidentified toxic contaminant or a larger quantity of psilocybin resulting in increased serotonergic activity. There may also be unidentified predisposing factors that contribute to the development of ATN following Psilocybe mushroom ingestion. For instance, the case of the 20-year-old feminine who developed AKI after the ingestion of “magic mushrooms” shares similarities to our case. Sadly, the identification of that mushroom is just not recognized.

This case identifies that there could also be potential for reversible nephrotoxicity following publicity to Psilocybe mushrooms. With supportive care, the AKI in our affected person resolved without sequelae.