Abstract
Kava plant root (piper methysticum) is an ingredient used in ceremonial drinks throughout Pacific and South Sea Island communities. Kava is made up of kavalactones; psychoactive compounds that act as central nervous system depressants. The rare occurrence of kavalactone toxicity manifests most commonly with hepatotoxicity, and cases of myoglobinuria have been reported. Our case describes an association of significant kava tea ingestion with acute tubulo-interstitial nephritis. An 18-year-old male, without any medical comorbidities, presented with oliguric acute kidney injury after ingesting 15 cups of kava tea. His creatinine at admission was 223umolL and peaked at 96 h post ingestion at 970umol/L despite intravenous fluid administration. His urine ACR was 196 mg/mmol, with microscopic haematuria; a creatinine kinase was 780 U/L, C3 was mildly reduced (0.77 g/L) with normal C4, and the remainder of a glomerulonephritis screen was negative. He did not have any evidence of hepatotoxicity but was bradycardic with a prolonged QT interval. A urine drug screen was negative for other substances. A kidney biopsy demonstrated severe acute tubulointerstitial nephritis without acute tubular necrosis or evidence of myoglobulin-related injury. He was commenced on oral corticosteroids and had complete recovery of his kidney function after 2 weeks, without requiring kidney replacement therapy. Toxicology analysis of the kava powder identified four different kavalactones without additional substances.