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Abstract: FR-OR54

Clinicopathologic Characteristics, Etiologies, and Outcomes of Secondary Oxalate Nephropathy

Session Information

Category: Pathology and Lab Medicine

  • 1800 Pathology and Lab Medicine

Authors

  • Nasr, Samih H., Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Valeri, Anthony M., Columbia University, New York, New York, United States
  • Said, Samar M., Olmsted County Medical Center, Rochester, Minnesota, United States
  • Sethi, Sanjeev, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Nath, Karl A., Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Lieske, John C., Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
  • Bu, Lihong, Mayo Foundation for Medical Education and Research, Rochester, Minnesota, United States
Background

The characteristics of secondary oxalate nephropathy (ON) are not well define, and the rate of recurrence after kidney transplant (Tx) and Tx outcome are unknown. We report the largest series on secondary ON to date

Methods

Retrospective analysis of clinicopathologic and outcome characteristics of 113 patients with secondary ON in the native kidney diagnosed at a large tertiary care academic center.

Results

Biopsy incidence was 0.97%. ON was attributed to enteric hyperoxaluria in 60% (most commonly RYGB), excessive ingestion of foods high in oxalate or oxalate precursors in 23% (most commonly vitamin C), and was idiopathic in 17%. Most patients presented with AKI (particularly in the ingestion group) or AKI on CKD, and 63% were diabetic. Calcium oxalate (CaOx) crystals were more abundant in the ingestion than enteric group, and were accompanied by acute tubular injury, inflammation, and interstitial fibrosis and tubular atrophy (IFTA). Concurrent pathologic conditions were present in 53%, most commonly diabetic nephropathy. After a median follow up of 36 months, 27% had kidney recovery, 19% had persistent kidney dysfunction, 54% developed kidney failure, and 29% died. The mean kidney survival was worse for patients with a concurrent pathologic lesion (30 vs. 96 months for those without, p<0.001). Independent predictors of kidney failure were degree of IFTA and nadir eGFR but not degree of crystal deposition. After a median follow up of 58 months in 23 patients who received kidney TX, 4 had graft loss (due to ON in 3). The 2-, 5-, and 10-year graft survivals were 90%, 79%, and 50%.

Conclusion

ON is a rare cause of AKI or AKI on CKD. Most patients have co-morbid pathologic conditions, particularly diabetic nephropathy, which worsen the prognosis. Recurrence in the renal allograft and graft loss may occur if hyperoxaluria is not controlled.

Abundant calcium oxalate crystals are seen under polarized light