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To the Editor:

We wanted to comment on a recent article in the American Journal of Transplantation: Elias N, et al Native Portal Vein Embolization for Persistent Hyperoxaluria Following Kidney and Auxiliary Partial Liver Transplantation [1].

In particular, we wanted to comment on the role of auxiliary liver transplant in the attempted treatment of primary hyperoxaluria. Such a treatment is not only ineffective, but dangerous because it exposes a patient to a major organ transplant (auxiliary liver transplant), which will not help correct their problem.

The error is in the misunderstanding about the metabolic defect of primary hyperoxaluria. Unlike many other genetic metabolic disease where genetic defects can be corrected with the transplantation of genetically normal hepatocytes, the problem with primary hyperoxaluria is completely different. With primary hyperoxaluria the genetically defective liver overproduces oxalate whose only mechanism of excretion is the kidney. The addition of genetically normal hepatocytes by transplantation will not correct this problem because the additional liver cells are not capable of metabolizing the excess oxalate. Because it will continue to overproduce oxalate, the genetically defective liver must be removed entirely since it is the source of this problem [2-4]. Therefore, an auxiliary liver transplant will not help in the treatment of primary hyperoxaluria and physicians and transplant surgeons would be well advised to avoid this procedure in the attempted treatment of primary hyperoxaluria.

  • J. F. Trotter1,* and D. Milliner2

  • 1 Baylor University Medical Center, Dallas, TX

  • 2 Mayo Clinic, Rochester, MN

  • *Corresponding author: James F. Trotter, james.trotter@baylorhealth.edu

Disclosure

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The authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation.

References

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