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-PO512

GOLD MARK "S": A Unique Cause of High-Anion Gap Metabolic Acidosis

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Allahrakha, Hassan H., Methodist Dallas Medical Center, Dallas, Texas, United States
  • Hazari, Akash, Methodist Dallas Medical Center, Dallas, Texas, United States
  • Collazo-Maldonado, Roberto L., Methodist Dallas Medical Center, Dallas, Texas, United States
Introduction

Calcific uremic arteriolopathy (CUA) is a serious disorder characterized by vascular calcifications that can affect patients with advanced chronic kidney disease. Currently, there is no approved therapy for CUA, but sodium thiosulfate (STS) has been used off-label for CUA. Mehta et. Al proposed a new anion gap mnemonic for the 21st century: GOLD MARK. TS is also a cause of high anion gap metabolic acidosis (HAGMA). We present two cases of STS-induced HAGMA.

Case Description

The first patient was a 58-year-old male with end-stage renal disease (ESRD) who presented with left toe gangrene. He was diagnosed with chronic CUA. He received STS (50 g) and underwent dialysis. Eleven days following admission, he developed HAGMA (anion gap: 27 mEq/L, CO2: 17 mEq/L). The second patient was a 32-year-old female with ESRD secondary to diffuse proliferative lupus nephritis who was admitted for central retinal artery occlusion. She was diagnosed with a painful ulcer on the right thigh secondary to CUA. She received STS and developed HAGMA during her hospitalization (anion gap: 22 mEq/L). In both cases, HAGMA resolved following discontinuation of STS.

Discussion

The mechanism of how STS causes HAGMA is unknown. It is presumed to be due to oxidation of thiosulfate to sulfate by the liver or intestinal bacteria, which is enhanced in patients with ESRD due to reduced clearance of the medication. A new HAGMA mnemonic has been proposed: GOLD MARK (Glycols [ethylene and propylene], Oxoproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, and Ketoacidosis). We propose that STS be considered in the differential diagnosis of HAGMA, and that “S” for STS be added to the end of the mnemonic GOLD MARK.