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Magic Mushrooms and Unexpected Toxicity with Severe AKI and Thrombosis

Acute kidney failure, Myocarditis Acute kidney failure, Myocarditis
Acute kidney failure, Myocarditis Acute kidney failure, Myocarditis

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Poster abstract

Acute kidney injury (AKI) secondary to toxin exposure is an uncommon but potentially life-threatening condition, particularly when associated with multisystem involvement. Psilocybin-containing mushrooms, also known as "magic mushrooms", are generally considered to have low systemic toxicity; however, rare cases of severe complications have been reported.

This case describes a middle-aged male with prior cardiovascular comorbidities and a history of recreational drug use who developed severe anuric AKI requiring dialysis following ingestion of magic mushrooms in combination with other substances. His course was complicated by supraventricular tachycardia (SVT), markedly elevated cardiac biomarkers, and severe left ventricular dysfunction suggestive of myocarditis. Subsequent imaging demonstrated extensive arterial thrombosis, leading to renal infarction and pulmonary embolism.

Despite intensive multidisciplinary management, the clinical course was progressive and ultimately fatal. This case highlights the potential for life-threatening complications from polysubstance use and underscores the need for heightened clinical vigilance regarding toxin-induced organ injury and prothrombotic states.

Complaints

The patient reported:

  • Nausea, general malaise, abdominal discomfort
  • Persistent retching (Involuntary, repetitive contractions of the stomach and diaphragm that mimic vomiting but do not produce expulsion of gastric contents)
  • Diarrhea, sweating, tachycardia, visual hallucinations
  • Reduced urine output

Symptoms began within hours after ingestion of magic mushrooms along with alcohol and lysergic acid diethylamide (LSD) that progressively worsened.

Anamnesis

Introduction

Psilocybin (4-phosphoryloxy-N,N-dimethyltryptamine; 4-PO-DMT) belongs to the class of naturally occurring tryptamine alkaloid. It is found in more than 200 mushroom species, mainly from the genera Panaeolina, Panaeolus, Conocybe, Gymnopilus, Stropharia, Psilocybe, and Pluteus. It has a long history of usage in Indigenous spiritual and ceremonial practices and is now gaining attention for its psychoactive properties and potential therapeutic applications.

After ingestion, psilocybin is quickly converted to psilocin, a serotonergic compound structurally same to serotonin. Psilocin acts primarily as a partial agonist at serotonin receptors, especially the serotonin 2A receptor (5-HT2A), altering activity in brain regions such as the prefrontal cortex and amygdala. This leads to effects including euphoria, visual and auditory hallucinations, perceptual changes, time distortion, and spiritual experiences.

Psilocybin-containing (“magic”) mushrooms are increasingly employed in both recreational settings and controlled therapeutic contexts due to their psychoactive effects. Available evidence from case series and toxicology reviews indicates that adverse events are most often neuropsychiatric, transient, and self-limiting, with serious systemic toxicity considered uncommon. However, rare but clinically significant reports have described the development of AKI following ingestion of hallucinogenic mushrooms, with some cases progressing to severe renal impairment requiring renal replacement therapy.

History

The patient was a middle-aged male with significant cardiovascular and metabolic comorbidities, including:

  • Hypertension
  • Peripheral vascular disease
  • Prior non-ST elevation myocardial infarction
  • Type 2 diabetes mellitus

He reported:

  • Recent ingestion of magic mushrooms along with alcohol and LSD
  • Past history of cocaine use (no recent intake confirmed)

There was:

  • No regular medication use
  • No known thrombophilia or autoimmune disease
  • No use of herbal or alternative therapies

The combination of polysubstance exposure and underlying vascular disease constituted a high-risk clinical background.

Examination

The patient was oligoanuric for approximately 4 days prior to hospital admission and remained anuric during hospitalization.

(a) Laboratory investigations

  • On admission, laboratory investigations showed elevated C-reactive protein (CRP; 112.8 mg/L) and white blood cell (WBC) count (12.47 ×10⁹/L).
  • Repeat investigations showed worsening inflammatory markers with CRP of 228.4 mg/L and WBC count of 18.91 ×10⁹/L.
  • Renal function tests showed elevated creatinine (482 µmol/L rising to 844 µmol/L) and urea (26.3 mmol/L rising to 41.5 mmol/L), with estimated glomerular filtration rate declining from 10 to 5.
  • Electrolyte abnormalities included potassium increasing from 5.3 to 6.2 mmol/L and phosphate increasing from 2.02 to 3.91 mmol/L.
  • Liver function tests showed elevated alanine aminotransferase (692 U/L decreasing to 172 U/L) with bilirubin within normal limits.
  • Troponin level was markedly elevated at 16,774 ng/L.

(b) Transthoracic echocardiography

  • SVT with a heart rate from 170 to 180 beats/minute with concurrent hypotension (90 mmHg systolic blood pressure).
  • Heart failure with reduced ejection fraction (about 35% ejection fraction) accompanied by a left ventricular mural thrombus/blood clot.

(c) Computed tomography imaging

  • Extensive thrombosis involving the abdominal aorta, iliac arteries, and superior mesenteric artery.
  • Right renal infarction due to renal arterial occlusion and pulmonary embolism involving the right lower lobe.
  • Ischemic changes in the descending colon.

(d) Additional workup

  • Negative autoimmune and thrombophilia screening.
  • The overall findings supported a diagnosis of severe toxin-associated AKI, suspected myocarditis, and widespread thrombotic complications with rectal bleeding and severe colicky abdominal pain.

Treatment

  • The patient was treated with intermittent hemodialysis due to persistent anuria and electrolyte disturbances.
  • He received oral co-amoxiclav for a possible chest infection.
  • During an episode of SVT, bisoprolol was administered followed by 3 doses of adenosine, which were unsuccessful.
  • Amiodarone loading dose and maintenance infusion were administered, resulting in rhythm control.
  • Therapeutic anticoagulation was initiated following identification of a left ventricular thrombus.
  • Oral prednisolone (30 mg once a day) was started for suspected myocarditis.
  • The patient required coronary care unit monitoring during clinical deterioration.
  • Following multidisciplinary team discussion, active treatment was withdrawn and palliative care was initiated.

Results

Discussion

This case shows a rare but severe form of toxin-related multiorgan injury. While most cases of psilocybin exposure are mild, this patient developed kidney failure, cardiac dysfunction, and widespread thrombosis.

Underlying vascular disease and prior substance use may have increased susceptibility to severe complications. The extent of thrombosis and organ damage is not typical for toxin-related AKI, which is often reversible.

Despite appropriate supportive and targeted treatment, the patient’s condition worsened, indicating a poor prognosis in such presentations.

Key learnings

  • Psilocybin-containing mushrooms can rarely cause severe and life-threatening multisystem toxicity.
  • Polysubstance use, particularly with agents such as LSD and cocaine, may amplify the risk of complications.
  • AKI with systemic manifestations should prompt thorough evaluation for toxin exposure.
  • Early identification of myocarditis and thrombotic complications is fundamental for timely management.
  • Multidisciplinary care is critical in tackling complex toxicological emergencies, although outcomes may remain poor in severe cases.

Source:

Cureus

Article:

Acute Kidney Failure and Myocarditis Triggered by Magic Mushroom Toxicity in a Patient With Prior Cocaine Exposure

Authors:

Aung Phyo Oo et al.

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