A teenager presenting with anuric acute renal failure and metabolic acidosis with a high anion gap: Questions
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CLINICAL QUIZ
A teenager presenting with anuric acute renal failure and metabolic acidosis with a high anion gap: Questions Çağla Serpil Doğan 1 & Gülşah Kaya Aksoy 1 & Kadir Aras Demircan 1 & Şenay Yıldırım 2 Received: 20 March 2020 / Accepted: 23 March 2020 # IPNA 2020
A 15-year-old boy was referred to our emergency department with a history of nausea, vomiting, and decreased urine output for 2 days. On his physical examination, his height and weight were 167 cm (50 percentile) and 58 kg (25–50 percentile), respectively. Blood pressure was 110/70 mmHg (95th percentile for age, gender, and height; 131/83 mmHg) with a heart rate of 75 beats per minute. He was clinically euvolemic and anuric at presentation. Other systemic examination findings were normal. There was no history of previous illness. Initial laboratory results revealed hepatic injury, rhabdomyolysis, and severe renal failure. Venous blood gas showed a pH of 7.28, HCO−3 of 18 mmol/l, PaCO2 of 44 mmHg, lactate of 0.8 mmol/l, and corrected anion gap of 21 mmol/l consistent with high anion gap metabolic acidosis. Despite the presence of severe renal failure, the corresponding serum potassium and phosphorus levels were inappropriately normal. Ultrasound of the urinary tract was found normal except for increased parenchymal echogenicity (grade 2) in both kidneys. A renal biopsy performed due to anuric acute renal failure
The answers to these questions can be found at https://doi.org/10.1007/ s00467-020-04552-0. * Çağla Serpil Doğan [email protected] 1
Department of Pediatrics, Division of Pediatric Nephrology, Antalya Training and Research Hospital, 07059 Antalya, Turkey
2
Department of Pathology, Antalya Training and Research Hospital, Antalya, Turkey
demonstrated the lesions including cytoplasmic vacuolization, nuclear alterations, single cell necrosis of epithelial cells as well as focal loss of brush border, and desquamation of epithelial cells into the tubular lumen, mostly affecting the proximal tubule. Mild interstitial inflammation was present. Vessels and glomeruli were not affected. These findings were considered as moderate acute tubular injury (Fig. 1a, b, c). In view of anuric renal failure, emergent hemodialysis was initiated and continued for 6 days. His urination began on the third hospital day and gradually increased, and his all laboratory findings progressively improved during the period of dialysis therapy. The first urine sample obtained on the 3rd day of admission showed glycosuria, nephrotic range proteinuria, uricosuria, and phosphaturia. After stopping dialysis, a normal anion gap hypercloremic metabolic acidosis, accompanied by positive urinary anion gap, developed in addition to indicatives of proximal tubular dysfunction. At that time, the patient who entered a period of polyuria was followed by fluid and electrolyte support and discharged
Pediatr Nephrol
Fig. 1 Acute tubular injury including necrotic epithelial cells in lumen, cytoplasmic vacuolization and single cell necrosis of epithelial cells with mild interst
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