A favorable outcome is more likely if a kidney transplant is complemented by a liver transplant, given the disease originates in the liver. Controversy
Perhaps the key difficulty in understanding pathogenesis of primary hyperoxaluria, or more specifically, why AGXT ends up in mitochondria instead of peroxisomes, stems from AGXTs somewhat peculiar evolution. Namely, prior to its current peroxysomal destiny, AGXT indeed used to be bound to mitochondria. AGXTs peroxisomal targeting sequence is uniquely specific for mammalian species, suggesting the presence of additional peroxisomal targeting information elsewhere in the AGT molecule. As AGXT was redirected to peroxisomes over the course of evolution, it is plausible  that its current aberrant localization to mitochondria owes to some hidden molecular signature in AGXTs spatial configuration unmasked by PH1 mutations affecting the AGXT gene. References
External links

GeneReviews/NIH/NCBI/UW entry on Primary Hyperoxaluria Type 1
It is mostly (96.6%) circulating in its original form; only a small proportion is metabolized by the liver enzymes UGT1A1 and UGT1A3, resulting in a glucuronide.The drug is mainly excreted via the faeces (93.3%). Less than 2% is found in the urine. Chemistry
Letermovir is used as the free acid. It is a white to off-white, amorphous powder that is slightly hygroscopic, very slightly soluble in water, and very soluble in acetonitrile, acetone, dimethylacetamide, ethanol, and 2-propanol.The molecule has one asymmetric carbon atom, which is in S configuration. References
External links
"Letermovir". Drug Information Portal. U.S. National Library of Medicine. "Letermovir Injection". MedlinePlus.