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Abstract: PO2128

Outcomes of Early and Late Calcium Oxalate Deposition Following Kidney Transplantation

Session Information

Category: Transplantation

  • 1902 Transplantation: Clinical

Authors

  • Nguyen, Thanh Thanh T., University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, United States
  • Astor, Brad C., University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, United States
  • Zhong, Weixiong, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, United States
  • Parajuli, Sandesh, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, United States
  • Aziz, Fahad, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, United States
  • Mohamed, Maha A., University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, United States
  • Djamali, Arjang, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, United States
  • Mandelbrot, Didier A., University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, United States
  • Garg, Neetika, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, United States
Background

Calcium oxalate deposition (CaOx) can result in progressive native kidney disease. The pathophysiology of hyperoxaluria in kidney transplant (KT) differs, especially early after surgery where the allograft encounters high levels. It is not clear whether CaOx in a kidney allograft portends worse outcomes. Determining its clinical relevance will influence the need for aggressive dietary or medication-based interventions.

Methods

All KT recipients at our center with CaOx on kidney allograft biopsy were categorized into two cohorts: delayed graft function (DGF; n=13) and late graft dysfunction (n=25). Up to 5 controls were selected per DGF case through event density sampling matched for organ type (kidney vs. simultaneous pancreas-kidney), prior transplants, and history of prolonged DGF prompting a biopsy (n=46). Controls for ‘late’ cases were matched for organ type, prior transplants, and living vs. deceased donor (n=125). Variables found to be statistically significantly associated with case status in bivariate analysis (p<0.10) were included in multivariate Cox regression analyses of allograft outcomes.

Results

DGF cases were more likely to have had gastric bypass surgery (7.7% vs. 0%, p=0.06) and less likely to have a history of rejection (7.7% vs. 37.0%, p=0.06) than controls. CaOx during DGF was not associated with increased risk of graft failure after adjustment (HR 1.1, p=0.87; Figure 1). ‘Late’ CaOx cases diagnosed median of 56.7 months (IQR: 9.8-108.9 months) after transplant were older at time of transplant (53.9 vs. 48.4 years, p=0.04) and less likely to be male (36% vs 61%, p=0.03) than controls. ‘Late’ CaOx was associated with a higher risk of allograft failure after adjustment (HR 3.2, p<0.001); Figure 2).

Conclusion

CaOx in kidney allograft during DGF may be a consequence of high circulating oxalate levels and was not associated with worse KToutcomes. ‘Late’ CaOx, likely related to increased intestinal oxalate absorption, a phenotype similar to secondary hyperoxaluria in native kidneys, was associated with increased risk of allograft failure.