Metabolic acidosis with increased anion gap, oxaluria, and acute kidney injury: Questions

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CLINICAL QUIZ

Metabolic acidosis with increased anion gap, oxaluria, and acute kidney injury: Questions Bagdagul Aksu 1,2 & Erkin Rahimov 3,4 Sevinc Emre 2 & Aydan Sirin 2

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Alev Yilmaz 2,5

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Zeynep Yuruk Yildirim 2,5

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Ilmay Bilge 2,6

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Received: 2 August 2020 / Revised: 2 August 2020 / Accepted: 2 September 2020 # IPNA 2020

Keywords Acute kidney injury . Metabolic acidosis . Ethylene glycol intoxicaton

Case summary A 17-year-old boy was admitted to a hospital with nausea and headache. His blood pressure was 140/100 mmHg, serum creatinine was 0.88 mg/dL, and white blood cell count was 11.6 × 103/mm3. After 4 h of follow-up, he was discharged from the emergency room as his blood pressure decreased to normal range for his age. Eight hours later, he was admitted to our pediatric emergency room with headache and somnolence. His previous medical history was unremarkable. According to his own statement, he smoked 3–4 cigarettes a day and never used drugs or alcohol. The patient was in a moderate overall condition and appeared drowsy. Systemic physical examination was

The answers to these questions can be found at https://doi.org/10.1007/ s00467-020-04758-2 * Bagdagul Aksu [email protected] 1

Department of Pediatric Basic Sciences, Institute of Child Health, Istanbul University, 34390 Istanbul, Turkey

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Division of Pediatric Nephrology, Istanbul Faculty of Medicine, Istanbul University, 34390 Istanbul, Turkey

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Department of Child Health and Diseases, Istanbul Faculty of Medicine, Istanbul University, 34390 Istanbul, Turkey

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Department of Child Health and Diseases, Baku Medical Plaza, Baku, Azerbaijan

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Institute of Child Health, Istanbul University, 34390 Istanbul, Turkey

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Division of Pediatric Nephrology, Koc University Hospital, Istanbul, Turkey

unremarkable. Vital signs were as follows: BP 180/100 mmHg (> 95th + 12 mmHg, stage 2 hypertension), HR 104 bpm, RR 20 bpm, and temperature which was 36.5 °C. His Glasgow Coma Scale score was 13/15. Neurological examination included cranial nerves and ophthalmoscopy and was unremarkable; pupils were equal and round, reactive to light. He was the second child of three, born to consanguineous parents. The mother had type 2 diabetes mellitus and the father had hypertension. The father worked in a car repair shop 2 days a week. Laboratory findings at the time of admission were as follows: white blood cell count was 18.7 × 103/mm3, hemoglobin 16.9 g/dL, platelets 236 × 103/mm3, urea 45.0 mg/dL, creatinine 1.2 mg/dL, glucose 88 mg/dL, sodium 140 mmol/L, potassium 5.4 mmol/L, chloride 102 mmol/L, calcium 9.7 mg/dL, phosphorus 3.3 mg/dL, total protein 7.8 g/dL, albumin 5 g/dL, C-reactive protein 3.8 mg/dL, ammonia 19 umol/L, and lactate 2.5 umol/L. There was metabolic acidosis (blood gas pH: 7.29, HCO3: 17 mmol/L, PCO2: 34.6 mmHg, BE: − 10.2 mmol/L). The anion gap was 26.4 mmol/L based on the formula [(Na+ + K+) − (Cl− + HCO3−)]. Calculated osmolarity was 293.5 mOsm/kg. Serum complement C3 (130.25 mg/dL) and C4 (23.8 mg/dL) were in the normal range. Serum co