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Kidney Week

Abstract: PO0305

Excess Vitamin C Leading to Hyperoxaluria and AKI

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Julian, Katherine, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Abendroth, Catherine, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Zebi, Ali Mohammed, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Karasinski, Amanda A., Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Jain, Rohit, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
Introduction

Secondary hyperoxaluria is caused by increased ingestion of oxalate or oxalate precursors, increased oxalate enteric absorption due to fat malabsorption, or changes in intestinal microflora and can manifest as end stage renal disease or hypothyroidism.

Case Description

A 55-year-old female with history of hyperparathyroidism and hypothyroidism (not med compliant) presented with myxedema coma secondary to uncontrolled hypothyroidism. Initial workup revealed elevated potassium (7mmol/L), BUN (194mg/dL), SCr (35mg/dL) and TSH (>100uIU/mL). She was given IV levothyroxine, IV liothyronine, insulin, calcium gluconate and hydrocortisone, and started hemodialysis in the setting of acute kidney injury (AKI) with no known underlying CKD, nephrolithiasis or nephrocalcinosis. Autoimmune, gastrointestinal, and hepatobiliary AKI etiologies were ruled out. A renal biopsy revealed renal oxalosis (Fig 1). Investigation of possible secondary causes of renal oxalosis revealed consumption of large quantities of vitamin C in hopes of preserving her health during the COVID-19 pandemic.The patient remained dependent on hemodialysis was discharged on levothyroxine 150mcg sublingual daily followed by nephrology and endocrinology. At time of discharge, TSH remained >100 uIU/mL, but free T4 was 0.86 ng/dL without any hypothyroid symptoms. High dose vitamin C consumption was discontinued.

Discussion

The combination of severe hypothyroidism resulting in myxedema coma and the excessive intake of vitamin C, a precursor for oxalate stones in the kidney, resulted in AKI. However, we believe the severe hypothyroidism was a result of medication noncompliance vs manifestation of systemic oxalosis. We recommend considering secondary oxalosis in cases of dialysis-dependent AKI in the setting of high dose vitamin C consumption or increased exogenous oxalate ingestion and confirming this diagnosis with renal biopsy.

Figure 1: Left: Rhomboid shaped calcium oxalate crystals distending renal tubule with attenuated and disruption of epithelial lining. Right: Calcium oxalate crystals characteristically birefringent under polarized light microscopy.