Abstract: FR-PO706
Little Stones, Big Trouble: Nutritional Oxalosis in a Child
Session Information
- Pediatric Nephrology - 1
October 25, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pediatric Nephrology
- 1900 Pediatric Nephrology
Authors
- Shi, Vivian, Stanford University, Stanford, California, United States
- Zhao, Xixi, Stanford University, Stanford, California, United States
Introduction
Oxalate nephropathy is a rare condition that results in acute kidney injury and chronic kidney disease. Although primary hyperoxaluria (PH) accounts for the majority of cases of oxalate nephropathy in pediatrics, our case highlights the importance in considering secondary causes. We present a case of a 9-year-old girl with kidney injury requiring dialysis due to nutritional oxalosis.
Case Description
A 9-year-old female with a history of failure to thrive presented with bilateral leg pain. Physical exam revealed extreme cachexia. Admission labs were notable for Na 101, K 6.6, BUN 157, and creatinine 8.56 (previous baseline 0.38 obtained 16 months prior), which prompted emergent hemodialysis (HD). Kidney biopsy showed diffuse oxalate crystals and severe interstitial fibrosis with tubular atrophy. Systemic oxalosis workup was negative. Genetic testing for PH was negative. A review of patient’s diet prior to illness revealed large consumption of many high oxalate containing foods, including nuts, spinach, chocolates, as well as daily vitamin C supplements. Elevated plasma oxalate levels normalized with maintenance HD and diet control. She continued on HD until kidney transplantation.
Discussion
The patient presented at a young age with sudden end stage kidney disease due to oxalate nephropathy. Differentiating PH from secondary hyperoxaluria is crucial in determining the treatment of choice. PH is a rare inborn error of glyoxylate metabolism that results in hepatic overproduction of oxalate, leading to increased urinary excretion and kidney disease. Secondary hyperoxaluria can result from increased dietary intake or enteric hyperoxaluria. This case highlights the need for genetic testing and considering secondary causes of hyperoxaluria in pediatrics. The case also emphasizes the need for regular monitoring of nutritional sources in pediatric patients with failure to thrive, since their diet may be high in a single nutritional compound such as oxalate.
Oxalate crystals