ESPE Abstracts (2024) 98 P2-71

ESPE2024 Poster Category 2 Diabetes and Insulin (35 abstracts)

Severe Acute Kidney Injury in an Adolescent with Diabetic Ketoacidosis

Kübra Şen Küçük 1 , Reyhan Deveci Sevim 1 , Hatice Feray Arı 2 , Tolga Ünüvar 1 & Ahmet Anık 1


1Aydın Adnan Menderes University Faculty of Medicine, Department of Pediatric Endocrinology, Aydın, Turkey. 2Aydın Adnan Menderes University Faculty of Medicine, Department of Pediatric Intensive Care, Aydın, Turkey


Introduction: Acute kidney injury (AKI) is a common complication in diabetic ketoacidosis (DKA). AKI in children with DKA is often mild and transient. Severe AKI is rare.

Case: A 14-year-old female presented with symptoms consistent with recent-onset diabetes mellitus, accompanied by abdominal pain, vomiting, and respiratory distress over the preceding two days. Physical examination revealed confusion with a Glasgow Coma Scale of 12, alongside signs of deep and rapid breathing, tachycardia, peripheral hypoperfusion, and severe dehydration. Laboratory investigations revealed severe diabetic ketoacidosis (DKA) with hyperglycemia (541 mg/dL), glucosuria-ketonuria, and metabolic acidosis (pH=6.81, HCO3=5.2 mmol/L). The initial serum electrolytes and renal function tests were within normal range. The patient admitted to pediatric intensive care unit and fluid resuscitation and IV insulin therapy commenced per DKA protocol; however, hyperchloremia and hypernatremia emerged by the 24th hour, necessitating adjustment of fluid composition by reducing the chloride content of the fluid. Subsequently, between the 24th and 60th hours, the patient developed oliguria, periorbital edema, azotemia, elevated creatinine (4.1 mg/dL) levels, and persistent metabolic acidosis. The patient responded favorably to fluid restriction and diuretic therapy and renal replacement therapy was not initiated. Despite resolution of DKA symptoms between the 60th and 92nd hours, metabolic acidosis persisted alongside normal urine output, attributed to hyperchloremia, acute kidney injury (AKI), and elevated lactate levels. Intravenous bicarbonate therapy was administered accordingly. On the 6th day of hospitalization, despite persistent high levels of serum creatinine (4.51 mg/dL), other laboratory parameters normalized. With the onset of polyuria and negative fluid balance, hydration was augmented. By the 14th day, polyuria subsided, kidney function tests were completely normalized and the patient discharged with complete recovery.

Conclusion: AKI is a common complication in DKA resulting from dehydration that can be treated with fluid therapy. In these patients, despite persistent elevation of creatinine and severe AKI, renal replacement therapy is generally not required, as kidney function is expected to return to normal with standard treatment.

Keywords: Type 1 diabetes mellitus, diabetic ketoacidosis, severe acute kidney injury

Volume 98

62nd Annual ESPE (ESPE 2024)

Liverpool, UK
16 Nov 2024 - 18 Nov 2024

European Society for Paediatric Endocrinology 

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