Ketamine Use as a Cause of CKD: A Case Series

Lina Alatta(New York Hospital Queens), Bruce Spinowitz(New York Hospital Queens), Ritesh Raichoudhury(New York Hospital Queens), Zainulabdeen S Al-saedi(New York Hospital Queens), Sheng Kuo(New York Hospital Queens), Mohammed A Miqdad(New York Hospital Queens)
Journal of the American Society of Nephrology
October 1, 2024
Cited by 0

Abstract

Background: Use of ketamine has been associated with urinary tract pathology, including contraction of urinary bladder and lower urinary tract obstruction, leading to secondary renal injury. Clinical presentation and image findings include contracted bladder, ureteral stricture, and hydronephrosis. Ketamine is excreted in bile and urine. It has been proposed that tissue damage is related to the duration of exposure and contact with ketamine metabolites in the urinary system, and that bladder wall is usually the first organ to present with lower urinary tract symptoms followed by the lower third of the ureter and renal pelvis .We present a series with history of ketamine abuse resulting in obstructive uropathy and chronic kidney disease. Methods: Chart review of deidentified patient records with history of ketamine abuse who presented to New York Presbyterian Queens Hospital The following features were extracted: baseline demographic data, serum creatinine , BUN, estimated glomerular filtration rate, and renal imaging. Results: Seven patients presented to the hospital with abnormal renal function and history of ketamine abuse, all with hydronephrosis on imaging. Six were Asian and one African American. They were predominantly female (5:1). The median age of presentation was 32 (range, 31-56) years. Three patients had hypertension. Serum creatinine, blood urea nitrogen, and estimated glomerular filtration rate were 2.2 mg/dL(range 1.03 to 3.07), 36.2 mg/dL (range 21.4 to 64.3), 34 cc/min (25 to 45), respectively. All had the following abnormalities: elevated liver enzymes (median alanine aminotransferase of 47.5 U/L ,aspartate aminotransferase of 65 U/L , and alkaline phosphatase of 1060 U/L ; bile duct dilation; bladder wall thickening with moderate to severe hydronephrosis. All required urological intervention (six patients had bilateral ureter stents and one patient had bilateral percutaneous nephrostomy). One patient required transient hemodialysis and one died. Conclusion: Our experience of Ketamine abuse is consistent with findings in the literature. Image findings of obstructive uropathy are typical and when present, is associated with chronic kidney disease. It is associated with high morbidities and requires frequent hospitalizations and procedures. Cases are likely underreported as most patients may not have symptoms.


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