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Peer-reviewedCC BY 4.0Frontiers in Endocrinology

Case Report: Refractory mixed acidosis with iatrogenic hyperchloremic acidosis in diabetic ketoacidosis

  • Jing Lin1
  • Jianjun Zheng2
  • Xiangjin Xu3
  • Chuan Zhou4
  • Guokai Yang5
  • Rongfeng Zhu1
5 affiliations
  1. 1Department of Endocrinology, The 95th Hospital of Putian
  2. 2Gastroenterology Department, The 95th Hospital of Putian
  3. 3Department of Endocrinology, 900th Hospital of the Joint Logistics Team
  4. 4Medical Imaging Department, The 95th Hospital of Putian
  5. 5Department of Nephrology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University
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Abstract

This case highlights a critical but easily overlooked complication of diabetic ketoacidosis (DKA) management—iatrogenic hyperchloremic acidosis superimposed on ketoacidosis—and demonstrates the role of the Δ gap (ΔAG − ΔHCO ₃ ⁻ ) in identifying refractory mixed acidosis. The “peripheral metabolic pool” hypothesis is proposed as a possible additional mechanism for persistent pH deterioration despite improvement in central metabolic parameters. A 32-year-old woman with type 2 diabetes presented with severe DKA (pH 6.974) after excessive durian and beer consumption. Despite initial improvement in glucose and ketone levels, her pH paradoxically worsened to 6.84 with progressive hyperchloremia (96.8 to 115 mmol/L), leading to acute heart failure, acute kidney injury , among others. The Δ gap=ΔAG-ΔHCO ₃ ⁻ <-6 suggested the possible coexistence of high anion-gap ketoacidosis and normal anion-gap hyperchloremic acidosis, consistent with a mixed acidosis. Urinary β ₂ -microglobulin >4000 μg/L indicated proximal tubular injury. Continuous renal replacement therapy (CRRT) was initiated at 14 hours after admission; acidosis was successfully corrected after 12 hours of CRRT, with gradual recovery of organ function. Recognition of mixed acidosis and timely individualized CRRT were important in breaking this patient’s vicious cycle. Clinicians should avoid excessive chloride load in DKA management and consider balanced crystalloids after initial resuscitation.

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Cite

BibTeXRIS
BibTeX
@article{lin2026case,
  title = {{Case Report: Refractory mixed acidosis with iatrogenic hyperchloremic acidosis in diabetic ketoacidosis}},
  author = {Jing Lin and Jianjun Zheng and Xiangjin Xu and Chuan Zhou and Guokai Yang and Rongfeng Zhu},
  journal = {Frontiers in Endocrinology},
  year = {2026},
  month = oct,
  doi = {10.3389/fendo.2026.1969157},
  url = {https://www.frontiersin.org/articles/10.3389/fendo.2026.1969157/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Case Report: Refractory mixed acidosis with iatrogenic hyperchloremic acidosis in diabetic ketoacidosis
AU  - Jing Lin
AU  - Jianjun Zheng
AU  - Xiangjin Xu
AU  - Chuan Zhou
AU  - Guokai Yang
AU  - Rongfeng Zhu
PY  - 2026
DA  - 2026/10/21
JO  - Frontiers in Endocrinology
DO  - 10.3389/fendo.2026.1969157
UR  - https://www.frontiersin.org/articles/10.3389/fendo.2026.1969157/full
AB  - This case highlights a critical but easily overlooked complication of diabetic ketoacidosis (DKA) management—iatrogenic hyperchloremic acidosis superimposed on ketoacidosis—and demonstrates the role of the Δ gap (ΔAG − ΔHCO ₃ ⁻ ) in identifying refractory mixed acidosis. The “peripheral metabolic pool” hypothesis is proposed as a possible additional mechanism for persistent pH deterioration despite improvement in central metabolic parameters. A 32-year-old woman with type 2 diabetes presented with severe DKA (pH 6.974) after excessive durian and beer consumption. Despite initial improvement in glucose and ketone levels, her pH paradoxically worsened to 6.84 with progressive hyperchloremia (96.8 to 115 mmol/L), leading to acute heart failure, acute kidney injury , among others. The Δ gap=ΔAG-ΔHCO ₃ ⁻ <-6 suggested the possible coexistence of high anion-gap ketoacidosis and normal anion-gap hyperchloremic acidosis, consistent with a mixed acidosis. Urinary β ₂ -microglobulin >4000 μg/L indicated proximal tubular injury. Continuous renal replacement therapy (CRRT) was initiated at 14 hours after admission; acidosis was successfully corrected after 12 hours of CRRT, with gradual recovery of organ function. Recognition of mixed acidosis and timely individualized CRRT were important in breaking this patient’s vicious cycle. Clinicians should avoid excessive chloride load in DKA management and consider balanced crystalloids after initial resuscitation.
SN  - 1664-2392
ER  -