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Kidney Week

Abstract: PO0038

Presentation and Outcome of Oxalate Nephropathy Without Known Genetic or Gastrointestinal Cause

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

  • Bolen, Erin E., Mayo Clinic Arizona, Scottsdale, Arizona, United States
  • Abdelmalek, Mina, Mayo Clinic Arizona, Scottsdale, Arizona, United States
  • Lieske, John C., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Keddis, Mira T., Mayo Clinic Arizona, Scottsdale, Arizona, United States
Background

Oxalate nephropathy (ON) is a frequent and often unexpected finding on kidney biopsy. This study aimed to characterize causes and outcomes in biopsy-proven ON not due to known enteric cause or primary hyperoxaluria (PH) in a multisite health system.

Methods

Cases were identified based upon diagnosis of ON on kidney biopsy between 2009 to 2020 without known enteric or primary cause.

Results

Thirty-four cases were identified with a median follow-up of 11.9 months. None had known fat malabsorption. Genetic testing for PH was negative in 11, and there was no clinical suspicion of PH in the rest. Likely causes of ON included documented high dietary oxalate (7, 21%), oral and/or IV vitamin C supplementation (7, 21%), ethylene glycol (3, 9%), and orlistat (1, 3%). No cause could be identified in 16 (47%). Table 1 shows variables across three etiologies: unknown cause, diet-related, and vitamin C. All cases except one had diffuse intratubular calcium oxalate deposition on biopsy. End stage kidney disease (ESKD) was present in 53%. AKI stage III at biopsy was predictive of ESKD at last follow-up (p<0.05). Treatments included low oxalate diet (29, 85%), calcium supplementation (18, 53%), pyridoxine (12, 35%), and prednisone taper (12, 35%). Diet-related ON appeared to have lower rates of AKI stage III at diagnosis (5, 67%), ESKD (3, 43%), and mortality (2, 29%) compared to vitamin C-related ON and ON of unknown etiology.

Conclusion

This is the largest study of ON not due to PH or enteric cause. The most common causes were high-oxalate diet and high-dose vitamin C. In 47% of cases no cause was identified. ESKD was common, and AKI severity at presentation predicted ESKD at last follow up. Cases attributed strictly to dietary excess may have better short and long term outcomes.

Table 1

Funding

  • Clinical Revenue Support