Abstract: SA-PO0324
Crystalline Clear: AKI from Sunflower Seed-Associated Oxalate Nephropathy
Session Information
- AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Edwards, Jordan, Alameda Health System, Oakland, California, United States
- Odabaei, Golaun, Alameda Health System, Oakland, California, United States
- Jain, Neha, Alameda Health System, Oakland, California, United States
- Manjunath, Veena, Alameda Health System, Oakland, California, United States
Introduction
Oxalate nephropathy (ON) is a crystalline nephropathy defined by decreased renal function and intratubular deposition of calcium oxalate crystals. Hyperoxaluria drives the pathophysiology of ON and may be primary or secondary. Early consideration of kidney biopsy is important to mitigate renal dysfunction and progression to CKD.
Case Description
A 39-year-old male with no medical history was admitted with one week of vomiting and low back pain. Vital signs were notable for hypertension. Examination showed an ill appearing man with dry mucous membranes; foley placement yielded minimal dark urine. Labs revealed stage 3 AKI with creatinine 19.7 mg/dL (baseline 1.1 mg/dL). Urinalysis was bland.
Volume resuscitation did not improve AKI, and renal ultrasound was unrevealing. Steroids were started for acute interstitial nephritis. Kidney biopsy revealed numerous intratubular birefringent calcium oxalate crystals on polarized light microscopy, with interstitial fibrosis and tubular epithelial cell injury, features consistent with ON.
Renal function and uremic encephalopathy improved after five sessions of hemodialysis. Creatinine improved to 2.3 mg/dL one week after discharge. Genetic testing for primary hyperoxaluria was negative. Additional history revealed a 15 year diet of copious sunflower seeds, amounting to 1200-1400 mg/day of oxalate.
Discussion
ON is a pathologic diagnosis characterized by intratubular deposition of calcium oxalate crystals. Hyperoxaluria may be primary (inherited disorders of glyoxylate metabolism) or secondary (enteric malabsorption, dietary excess, toxins, medications).
In this case, gastrointestinal illness superimposed on chronic dietary oxalate excess likely caused urinary oxalate supersaturation, tubular obstruction, and AKI. Oxalate rich foods known to cause secondary ON include leafy vegetables, nuts, and coffee.
Early recognition of ON is important to enhance the chance of renal recovery.