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Kidney Week

Abstract: PO0310

Precipitous AKI: A Unique Form of AKI by Vancomycin

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Khalid, Sheikh Bilal, Shaukat Khanum Memorial Cancer Hospital and Research Centre, Lahore, Punjab, Pakistan
  • Mahmood, Javaria, Shalimar Medical and Dental College, Lahore, Pakistan

Vancomycin-associated acute kidney injury (VA-AKI) is a well-known entity. With improvement in formulations of vancomycin (vanc), its incidence has decreased, however it remains a risk factor of AKI especially when used in combination with other nephrotoxic agents. We present a case of VA-AKI that represents a unique pattern of kidney injury, known as “precipitous AKI".

Case Description

A 23-yr-old male presented to the emergency room with fever & body aches for 1 day. He was getting chemotherapy for acute lymphocytic leukemia; last received cyclophosphamide 10 days ago. He was tachycardic. Physical exam was unremarkable. His absolute neutrophil count was 0.5x103 cells/μl. He was admitted & started on IV vanc & Piperacillin/Tazobactam. On the 4th day of admission (DoA), he developed AKI with rise in blood urea nitrogen (BUN) and creatinine (Cr) to 37mg/dL and 3.6mg/dL, (baseline of 12mg/dL & 0.9mg/dL) respectively. Urine sediment showed granular casts suggestive of tubular injury. Vanc was stopped; until then he had received a cumulative dose of 5grams. Cr peaked to 8mg/dL on the 8th DoA. The rise in BUN was discordant which only rose to 52mg/dL. The patient never developed oliguria either. His BUN and Cr improved thereafter and he was discharged. The BUN and Cr were normal on repeat testing done 2 weeks later.


Precipitous AKI is the term coined by Velez et al. which appears to be the first description of this entity. To our knowledge, only a handful of cases have been reported. It is seen in patients who receive high cumulative dose of vancomycin and manifests as rapid rise in Cr (more than 2.5mg/dL in a day) while in other causes of AKI the rise of Cr is between 1-1.5mg/dL. The relative rise in BUN does not match that of Cr. The patients do not develop oliguria, & cystatin C is usually normal:. These observations support the notion that glomerular filtration is not affected, and is postulated to be caused by tubular toxicity that effects the tubular secretion of Cr. Further studies are needed however.