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

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: SA-PO267

Holy “Molly!” An Intriguing Case of AKI

Session Information

  • Trainee Case Reports - VI
    October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Chamarthi, Gajapathiraju, University of Flroida, Gainesville, Florida, United States
  • Lee Loy, Justin, University of Flroida, Gainesville, Florida, United States
  • Koratala, Abhilash, University of Flroida, Gainesville, Florida, United States
Introduction

Molly is the slang for ‘molecular’, which refers to the powder or crystal form of the synthetic psychoactive drug MDMA (3,4-methylenedioxymethamphetamine). Molly is often mixed with other drugs and substances such as bath salts (e.g. 4-methyl-apyrrolidinohexanophenone) and is not safe. While urine toxicology can detect amphetamines, current drug screens do not typically detect bath salts and other contaminants. MDMA can lead to severe hyperthermia, hyponatremia, liver, kidney and cardiovascular failure. Herein, we present a case of severe AKI in a Molly abuser.

Case Description

A 41-year-old man with a history of polysubstance abuse including alcohol, cocaine and molly presented to our institution with abdominal pain and vomiting. He has been taking molly prior to presentation and urine drug screen was positive for amphetamine. Labs showed AKI with a serum creatinine of 9 mg/dL (baseline 0.9), hyperkalemia (K 7 mmol/L) and hyperphosphatemia (P 18 mg/dL). Serum sodium was relatively normal (134 mmol/L). Serum creatine kinase (CPK) was elevated at 6814 U/L (Ref: 5-180). UA showed large blood on dipstick with 5 RBC/hpf consistent with myoglobinuria. Imaging excluded obstructive nephropathy and he was treated with intravenous hydration and supportive care. His renal function improved gradually over next several days.

Discussion

AKI associated with MDMA is primarily attributable to rhabdomyolysis, which could result from direct myocyte toxicity or seizures from symptomatic hyponatremia. Excessive physical exertion in the setting of inadequate water intake and impaired thermoregulation often complicates the picture. Direct tubulotoxicity, necrotizing vasculitis and malignant hypertension are other mechanisms of AKI. Rarely, it can cause bladder neck dysfunction leading to obstructive nephropathy. In addition, bath salts that contaminate molly can cause ATN and rhabdomyolysis. In addition to tubular toxicity, our patient could have had more severe rhabdomyolysis prior to presentation leading to pigment-induced AKI though the presentation CPK was not very high. It is also not certain whether his kidney injury is a result of MDMA alone or related to bath salts/other contaminants as well. Clinicians need to consider all these possibilities while evaluating patients with AKI and suspected drug abuse. History may not be always clear, especially in obtunded patients.