Excess vitamin c leading to hyperoxaluria and AKI

ABSTRACT

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.