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Kidney Week

Abstract: FR-PO209

An Uncommon Presentation of Cocaine-Induced Acute Interstitial Nephritis

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Bakshi, Dhruv, Saint Vincent Hospital, Worcester, Massachusetts, United States
  • Phachu, Deep, Saint Vincent Hospital, Worcester, Massachusetts, United States
Introduction

Cocaine induced kidney injury may occur through multiple mechanisms including rhabdomyolysis, thrombotic microangiopathy, glomerulonephritis, vasculitis, and renal infarction. Acute interstitial nephritis (AIN) is characterized by inflammatory infiltrates in the kidney interstitium sparing the glomeruli, that may occur from systemic autoimmune disorders, infection or drug-related mechanisms. Cocaine-induced AIN is a rare entity that has been poorly studied.

Case Description

A 45-year-old male was brought to the ER after being found unresponsive. He had acute kidney injury with a creatinine of 4, lactic acidosis, creatine kinase greater than 40,000 IU/L and urine toxicology positive for cocaine. Manual urine microscopy showed occasional non-dysmorphic RBCs and no WBCs. The patient was treated with IV fluids without renal replacement therapy. After regaining consciousness, he communicated a prolonged history of cocaine use but no kidney injury. He was treated for myoglobin-related toxic kidney injury from rhabdomyolysis.
Over the next few days, his creatinine plateaued around 4 despite volume resuscitation. On hospital day 15, a kidney biopsy revealed acute tubular injury with myoglobin casts, and prominent interstitial edema with inflammation suggestive of interstitial nephritits. This was presumed to be cocaine-induced AIN.

Discussion

The most common presentation of AIN is rash and fever (25-40%), with laboratory findings of acute kidney injury, eosinophilia (35-60%) and sterile pyuria (75-85%). The classical triad of fever, eosinophilia and AKI are present in <10% of all cases. A definitive diagnosis is made by a kidney biopsy which shows interstitial infiltrates and edema. In our patient, while diagnosis was confirmed with a classical picture on biopsy, the patient did not have any evidence of pyuria or eosinophils. This suggests that in a patient with cocaine overdose who shows non-improvement in creatinine, interstitial nephritis may be considered despite absence of classical clinical findings.