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: TH-PO0498

Metformin and Mayhem: How to Corral the Chaos

Session Information

Category: Dialysis

  • 801 Dialysis: Hemodialysis and Frequent Dialysis

Authors

  • Ijaz, Nadia, University of Maryland Medical System, Baltimore, Maryland, United States
  • King, Joshua D., University of Maryland Medical System, Baltimore, Maryland, United States
  • Hanouneh, Mohamad A., The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • MacDonald, Victoria A, University of Maryland Medical System, Baltimore, Maryland, United States
Introduction

Metformin, the most prescribed glucose lowering medication worldwide, has been used for more than six decades to manage diabetes. Introduced in Europe in the late 1950’s, it made its way to the US in 1995 after intense scrutiny due to the concern for lactic acidosis.

Case Description

A 75-year-old man with type 2 diabetes and end stage kidney disease on hemodialysis (HD) thrice weekly presented to the emergency room with altered mental status after missing two HD sessions. He was oriented to person only but otherwise hemodynamically stable. Laboratory results are listed in Fig 1. His wife reported he had been independently taking metformin 1000 mg twice daily for two months due to uncontrolled hyperglycemia, despite it being stopped when HD was started.
He was diagnosed with metformin induced lactic acidosis (MILA). He was initiated on emergent HD with blood flow rate 500 ml/min and dialysate flow rate 800 ml/min for four hours followed by continuous renal replacement therapy with another session of HD the following day. As a result, his lactic acidosis normalized, and his mental status returned to baseline. His metformin level later came back as 40 mcg/ml (therapeutic level 1-2 mcg/ml).

Discussion

Metformin in excess, inhibits oxidative phosphorylation promoting increased pyruvate conversion to lactate resulting in significant elevations. Patients may present with MILA where high levels of metformin are the primary cause of toxicity or metformin associated lactic acidosis (MALA) when there is another cause of lactic acidosis and metformin amplifies the degree of lactic acidosis.
Patients with metformin toxicity may present with preserved hemodynamics but can progress to shock requiring hemodynamic support. Dialysis should be initiated when lactate level > 15mmol/L or pH ≤ 7.1. HD is preferred initially, even with hemodynamic instability, due to rapid correction of acidosis, lactate, and removal of metformin, which subsequently improves hemodynamics. Bicarbonate administration should be avoided unless serum bicarbonate is < 5 mEq/L due to increased lactate generation.

Digital Object Identifier (DOI)