ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2023 and some content may be unavailable. To unlock all content for 2023, please visit the archives.

Abstract: TH-PO067

A Case of Rhabdomyolysis and Acute Tubular Necrosis with Lower than Expected Creatinine Kinase Level in a Patient with Cocaine Abuse

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials


  • Adhikari, Pabitra, Ascension Saint Francis, Evanston, Illinois, United States
  • Kishmiryan, Armen, Ascension Saint Francis, Evanston, Illinois, United States
  • Ramachandran, Akshaya, Ascension Saint Francis, Evanston, Illinois, United States
  • Ali, Mustafa, Ascension Saint Francis, Evanston, Illinois, United States

Clinicians rely on serum creatinine kinase (CK) levels to assess the severity of rhabdomyolysis (RM) and predict the development of acute kidney injury (AKI). It is widely accepted that rhabdomyolysis with CK levels less than 5000 U/L is unlikely to cause AKI. We report a case of cocaine induced rhabdomyolysis and subsequent development of myoglobinuric acute tubular necrosis (ATN) in a young healthy male with CK levels of 928 U/L at presentation.

Case Description

A 33-year-old male with a past medical history of poly-substance abuse presented with headache following intake of crack cocaine three days prior to the presentation. Examination were remarkable for blood pressure of 171/108 mmHg and dry mucous membranes. Laboratory studies were significant for serum creatinine (Cr) of 21 mg/dl, Blood Urea Nitrogen (BUN) of 113 mg/dl and CK of 928 U/L. Urine sample obtained after bladder catheterization revealed gross blood with 3-5 red blood cells (RBCs)/hpf, proteinuria of 100 mg/dl and the urine toxicology was positive for cocaine. Renal ultrasound was non-contributory. Patient did not meet the criteria for urgent dialysis and the patient was started on intravenous (IV) fluids. The patient remained anuric. All the work ups done for etiologies of AKI were negative. Renal biopsy was consistent with diffuse ATN with myoglobin casts. Outpatient follow-up and continued supportive treatment resulted in resolution of ATN and normal kidney function.


Cocaine induced RM can be traumatic due to seizure and/or hyperpyrexia and non-traumatic due to direct toxic effects of cocaine on skeletal muscle. CK and myoglobin levels change in parallel and CK levels correlate well with the severity of RM but its correlation and property to predict development of AKI is less reliable compared to serum myoglobin levels.

Figure showing Myoglobin Casts