Abstract: SA-PO0084
Transcutaneous Diethylene Glycol: An Unrecognized Cause of Anion Gap Acidosis with Osmolal Gap Complicated by Rapid Progression to ESRD
Session Information
- AKI: Clinical Diagnostics and Biomarkers
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Correa, Tatiana, Baystate Medical Center, Springfield, Massachusetts, United States
- Braden, Gregory Lee, Baystate Medical Center, Springfield, Massachusetts, United States
- Rennke, Helmut G., Harvard University, Cambridge, Massachusetts, United States
Introduction
Diethylene glycol (DEG) can cause anion gap acidosis (AGA) with an osmolal gap . It is in chafing, brake fluids & industrial solvents & inadvertently in pediatric medications. We present a case of DEG toxicity from unrecognized repeated transcutaneous solvent exposure causing significant AKI and AGA with interstitial and endothelial injury rapidly progressing to ESRD.
Case Description
A normotensive 32 year old male presented with AGA with these electrolytes in mEq/L: Na 141, K 5, Cl101, Bicarb 15, AG 25 & serum creatinine (Scr) of 2.1mg /dl, serum osmolal gap (OG) of 20 mOsm/kg, normal lactic acid, beta-hydroxybutyrate & negative toxic screen. Urinalysis showed a Total Protein/creat ratio of 4.9 g/g & granular casts. Biopsy on light microscopy showed segmental mesangial matrix expansion and capillary loop collapse. The interstitium had tubules with cytoplasmic vacuolization with 50% interstitial fibrosis & severe arteriolosclerosis. On immunofluorescence there were no immune deposits. Electron microscopy revealed widespread foot process effacement with swollen endothelial cells with degeneration and loss of fenestrations. After 16 months, Scr was 5.7 mg/dl & 4 months later dialysis was initiated.
Discussion
DEG toxicity presents with an initial phase of GI symptoms, followed by renal dysfunction and, late neurological effects. DEG increases the OG by approximately 0.9 mOsm/L for every 10 mg/dL with AGA due to hydroxyethoxyacetic acid and diglycolic acid.
The best mnemonic for AGA is GOLDMARK rather than MUDPILES as it includes “G” for glycols, which encompasses DEG. Our patient rapidly progressed to ERSD and only after chronic hemodialysis was the DEG toxicity recognized.
In a study of 32 DEG survivors, 18-month follow-up data showed that 9 of 26 patients required dialysis, and 13 had stage 3a or worse kidney disease.
Our case shows DEG toxicity not only causes interstitial fibrosis but also causes severe acute tubular necrosis. We for the first time show DEG can also cause extensive glomerular damage manifested as arteriolosclerosis, glomerular collapse & endothelial damage, new findings for DEG toxicity.
Our case demonstrates that DEG is often not recognized as a cause of AGA with an increased OG which can rapidly lead to ESRD.