MON-643 Unintended Ramifications: Burnt-Out Diabetes

Abstract Disclosure: M. Russe-Russe: None. E. Fernandez-Nuñez: None. L. Cruz-Rivera: None. J. Bosques-Lorenzo: None. S. Rodriguez-Perez: None. Burnt-Out Diabetes (BOD) is a phenomenon that occurs in diabetic patients on hemodialysis (HD) characterized by spontaneous improvement of glycemic levels requiring a decrease or complete cessation of antidiabetic medications. In principle, the proposed pathophysiology is that HD uses a semipermeable membrane (SPM) and concentration gradient to exchange dialysate and blood substances in the dialyzer, removing toxins and maintaining the electrolyte balance effect. In addition, plasma glucose diffuses across the SPM and concentration gradient from the bloodstream to the dialysate, leading to a decrease in plasma glucose concentration of the dialysate thought to be by diffusion of plasma glucose into erythrocytes. Other contributors are decreased renal and hepatic insulin clearance on HD, a decline in renal gluconeogenesis, deficient catecholamine release and impaired counterregulatory hormone response that raise blood glucose. This is the case of a 61 year old female presented to the ED with chest pain that was admitted due to an NSTEMI. Upon additional inquiry of medical history and home medications, she disclosed having T2DM but was not using antidiabetic medication at the time of admission. During hospitalization, HbA1c was 5.8%, she continued HD without requiring antidiabetic medication. Patient was diagnosed with Gestational Diabetes at age 29 but progressed to T2DM at age 45 and was managed with Metformin and Insulin at that time. Despite trying to maintain glycemic control she developed microvascular complications including Diabetic Nephropathy leading to HD. After three years of HD, she was weaned off from her antidiabetic medications due to experiencing several hypoglycemic events, eventually achieving normoglycemia, exhibiting BOD phenomenon. Despite not having clinical T2DM, she remained with microvascular complications managed by the respective subspecialties.The purpose of this case report is to increase the awareness and mechanism of BOD phenomenon, to shed some light on the importance of identifying the population that develops BOD and the challenges they meet while exhibiting hypoglycemic episodes increasing the risk of mortality. While the BOD phenomenon does not occur in every T2DM on HD; recognizing those that do can help prevent hypoglycemic events, the mortality and morbidity associated with and avoiding polypharmacy and health cost. Presentation: Monday, July 14, 2025

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Journal
Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.1003
Primary Topic
Diabetes Management and Research
Type
article
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article

MON-643 Unintended Ramifications: Burnt-Out Diabetes

Jaymilitte Bosques-Lorenzo, Mariaisabel Russe-Russe, Euri Fernandez-Nuñez, Luis J Cruz-Rivera et al.
Journal of the Endocrine Society
Diabetes Management and Research
article

MON-643 Unintended Ramifications: Burnt-Out Diabetes

Jaymilitte Bosques-Lorenzo, Mariaisabel Russe-Russe, Euri Fernandez-Nuñez, Luis J Cruz-Rivera, Leosbel Hurtado-Cabrera, Sarahi Rodriguez-Perez
article en

Abstract

Abstract Disclosure: M. Russe-Russe: None. E. Fernandez-Nuñez: None. L. Cruz-Rivera: None. J. Bosques-Lorenzo: None. S. Rodriguez-Perez: None. Burnt-Out Diabetes (BOD) is a phenomenon that occurs in diabetic patients on hemodialysis (HD) characterized by spontaneous improvement of glycemic levels requiring a decrease or complete cessation of antidiabetic medications. In principle, the proposed pathophysiology is that HD uses a semipermeable membrane (SPM) and concentration gradient to exchange dialysate and blood substances in the dialyzer, removing toxins and maintaining the electrolyte balance effect. In addition, plasma glucose diffuses across the SPM and concentration gradient from the bloodstream to the dialysate, leading to a decrease in plasma glucose concentration of the dialysate thought to be by diffusion of plasma glucose into erythrocytes. Other contributors are decreased renal and hepatic insulin clearance on HD, a decline in renal gluconeogenesis, deficient catecholamine release and impaired counterregulatory hormone response that raise blood glucose. This is the case of a 61 year old female presented to the ED with chest pain that was admitted due to an NSTEMI. Upon additional inquiry of medical history and home medications, she disclosed having T2DM but was not using antidiabetic medication at the time of admission. During hospitalization, HbA1c was 5.8%, she continued HD without requiring antidiabetic medication. Patient was diagnosed with Gestational Diabetes at age 29 but progressed to T2DM at age 45 and was managed with Metformin and Insulin at that time. Despite trying to maintain glycemic control she developed microvascular complications including Diabetic Nephropathy leading to HD. After three years of HD, she was weaned off from her antidiabetic medications due to experiencing several hypoglycemic events, eventually achieving normoglycemia, exhibiting BOD phenomenon. Despite not having clinical T2DM, she remained with microvascular complications managed by the respective subspecialties.The purpose of this case report is to increase the awareness and mechanism of BOD phenomenon, to shed some light on the importance of identifying the population that develops BOD and the challenges they meet while exhibiting hypoglycemic episodes increasing the risk of mortality. While the BOD phenomenon does not occur in every T2DM on HD; recognizing those that do can help prevent hypoglycemic events, the mortality and morbidity associated with and avoiding polypharmacy and health cost. Presentation: Monday, July 14, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
Larkin Community Hospital (US), San Juan City Hospital (PR), Bayamón Central University (PR)
Openalex Percentile: Top 60%
Diabetes Management and Research
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