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Kidney Week

Abstract: TH-PO710

Secondary IgA Nephropathy Due to Ketamine-Induced Cirrhosis: A Rare Cause of ESKD in Ketamine Users

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Bhenswala, Prashant N., Northwell Health, New Hyde Park, New York, United States
  • Sharma, Purva D., Northwell Health, New Hyde Park, New York, United States
Introduction

Ketamine abuse is a known cause of hepatobiliary injury and cirrhosis as well as urologic injury possibly resulting from irritation of the urologic system. Chronic ketamine use is also known to cause cystitis, bladder dysfunction, and hydronephrosis. The relationship between cirrhosis and IgA nephropathy is well known and is due to the liver’s inability to clear circulating IgA immune complexes. However, little to no reports linking Ketamine-Induced-Cirrhosis (KIC) to IgA nephropathy resulting in kidney failure and end-stage kidney disease needing dialysis have been reported.

Case Description

Our case involves a 26-year-old female with history of ketamine abuse (since age 16), with biopsy proven ketamine-induced liver injury with F1 fibrosis. She presented to the hospital with advanced kidney disease with a serum creatinine of 9 mg/dL, hematuria, and 1gm of proteinuria. Serologic workup was negative. Kidney biopsy was performed that showed focal crescentic and diffuse sclerosing glomerulonephritis consistent with IgA nephropathy with mild activity and severe chronicity. There was severe tubular atrophy and interstitial fibrosis. She was initiated on dialysis and remained dialysis dependent. As a result of her continued ketamine abuse, she was deemed to be ineligible for liver/kidney transplant.

Discussion

Ketamine is a known cause of urologic injury including decreased bladder compliance and volume, hematuria and rarely hydronephrosis and papillary injury. Our patient who was a chronic ketamine user developed progressive IgA nephropathy with crescentic and diffuse sclerosing glomerulonephritis with severe tubular atrophy, causing her to develop end stage kidney disease. This was thought to be secondary to ketamine induced cirrhosis. To the best of our knowledge, this cause of ESRD in ketamine users has not been reported. There should be a low threshold to perform kidney biopsy in ketamine misusers at the earliest onset of kidney disease. Treatment of secondary IgA nephropathy in ketamine users would include cessation of the drug and control of BP and proteinuria. Unfortunately, our patient continued to misuse ketamine and ended up with liver cirrhosis and end stage kidney disease.