Aminoaciduria and metabolic dysregulation during diabetic ketoacidosis: Results from the diabetic kidney alarm (DKA) study

Isabella Melena, Federica Piani, Kalie L. Tommerdahl, Cameron Severn, Linh T. Chung, Alexis MacDonald, Carissa Vinovskis, David Cherney, Laura Pyle, Carlos A. Roncal-Jimenez, Miguel A. Lanaspa, Arleta Rewers, Daniël H. van Raalte, Gabriel Cara-Fuentes, Chirag R. Parikh, Robert G. Nelson, Meda E. Pavkov, Kristen J. Nadeau, Richard J. Johnson, Petter Bjornstad*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Objective: We examined changes in the excretion of various amino acids and in glycolysis and ketogenesis-related metabolites, during and after diabetic ketoacidosis (DKA) diagnosis, in youth with known or new onset type 1 diabetes (T1D). Methods: Urine samples were collected from 40 youth with DKA (52% boys, mean age 11 ± 4 years, venous pH 7.2 ± 0.1, blood glucose 451 ± 163 mg/dL) at 3 time points: 0–8 h and 12–24 h after starting an insulin infusion, and 3 months after hospital discharge. Mixed-effects models evaluated the changes in amino acids and other metabolites in the urine. Results: Concentrations of urine histidine, threonine, tryptophan, and leucine per creatinine were highest at 0–8 h (148.8 ± 23.5, 59.5 ± 12.3, 15.4 ± 1.4, and 24.5 ± 2.4% of urine creatinine, respectively), and significantly decreased over 3 months (p = 0.028, p = 0.027, p = 0.019, and p < 0.0001, respectively). Urine histidine, threonine, tryptophan, and leucine per urine creatinine decreased by 10.6 ± 19.2, 0.7 ± 0.9, 1.3 ± 0.9, and 0.5 ± 0.3-fold, respectively, between 0 and 8 h and 3 months. Conclusions: In our study, DKA was associated with profound aminoaciduria, suggestive of proximal tubular dysfunction analogous to Fanconi syndrome.

Original languageEnglish
Article number108203
JournalJournal of Diabetes and its Complications
Issue number6
Early online date2022
Publication statusPublished - Jun 2022

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