This involves no radiation, no needles and no contrast agents that may cause allergic reactions. This test has good sensitivity and specificity.Typically duplex ultrasound scan is the only investigation required for decision making in carotid stenosis as it is widely available and rapidly performed. However, further imaging can be required if the stenosis is not near the bifurcation of the carotid artery.One of several different imaging modalities, such as a computed tomography angiogram (CTA) or magnetic resonance angiogram (MRA) may be useful. Each imaging modality has its advantages and disadvantages - Magnetic resonance angiography and CT angiography with contrast is contraindicated in patients with chronic kidney disease, catheter angiography has a 0.5% to 1.0% risk of stroke, MI, arterial injury or retroperitoneal bleeding. The investigation chosen will depend on the clinical question and the imaging expertise, experience and equipment available.For purpose of treatment, the degree of carotid stenosis is defined as:
percent stenosis = ( 1 − ( minimum diameter within stenosis) / ( poststenotic diameter ) ) × 100%. Screening
The U.S. Preventive Services Task Force (USPSTF) recommends against routine screening for carotid artery stenosis in those without symptoms as of 2021.While routine population screening is not advised, the American Heart Association and the Society for Vascular Surgery recommend screening in those diagnosed with related medical conditions or have risk factors for carotid artery disease.
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