A Rare Case of Magic Mushroom (Psilocybin) Related AKI and Hypertensive Emergency

A 31-year-old woman with well-controlled hypertension and metabolic syndrome developed acute kidney injury and a hypertensive emergency after ingesting psilocybin mushrooms. Her blood pressure reached 210/140, she experienced transient visual loss, and her troponin was elevated above 6000. Laboratory tests showed serum creatinine rising from a baseline of 0.9 to 4.6 mg/dL, proteinuria, and microscopic hematuria. A renal biopsy revealed vascular-predominant acute thrombotic microangiopathy. She was managed conservatively and did not require dialysis, but her kidney function only partially recovered, leaving a new baseline creatinine of 2.2-2.4 mg/dL and chronic kidney disease. Psilocybin can cause acute kidney injury leading to chronic kidney disease and secondary hypertension, possibly through vasoconstriction and endothelial damage.

Study at a glance

Abstract

Introduction: Magic (Psilocybin) mushrooms are used as hallucinogens, renal dysfunction as a rare side effect has been reported in literature. We chronicle a rare case of acute kidney injury and hypertensive emergency precipitated by psilocybin ingestion in a young female. Case Description: A 31-year-old female with good overall health and medical history of well controlled Hypertension (HTN) and metabolic syndrome presented with AKI in the setting of hypertensive emergency. Initial blood pressure (BP) on presentation was 210/140, with transient visual loss and elevated troponin >6000. Her other past medical history was significant for nephrolithiasis and COVID-19 few months ago. Physical examination was significant for HTN; no significant edema was present. Remaining physical examination was unremarkable. Laboratory evaluation demonstrated serum creatinine 4.6 mg/dL (baseline creatinine 0.9 mg/dL), 24-hr urine protein 920 mg/g, and serum albumin 3.0 g/dl. A blood film revealed occasional schistocytes. Urinalysis showed proteinuria and microscopic hematuria. Urine toxicology screen was negative. Routine blood and urine cultures showed no growth. Her serology, infectious disease workup and workup for paraproteinemia were inconclusive. Workup for secondary hypertension was negative. Computed tomography of the brain in the setting of transient visual loss, and ultrasound of the kidneys and bladder were unremarkable. Her transthoracic echo (TTE) showed severe concentric left ventricular hypertrophy, with grade II diastolic dysfunction. Renal biopsy showed features suggestive of vascular-predominant acute thrombotic microangiopathy. Patient was managed conservatively and did not require renal replacement therapy. Her serial follow up labs from last several months revealed the new baseline creatinine of 2.2-2.4 mg/dl, resulting in CKD as a sequel of partial recovery from AKI in the setting of psilocybin poisoning. Discussion: Psilocybin use can be associated with AKI leading to CKD and secondary hypertension. Mechanisms of renal injury are thought to be secondary to vasoconstricting effects and endothelial reaction, which needs to be further investigated. Nephrologists and primary providers should be vigilant to identify this rare cause of AKI.