One historical example of a private organization using this model is LifeSharers, which is free to join and whose members agree to sign a document giving preferred access to their organs. "The proposal [for an organ mutual insurance pool] can be easily summarized: An individual would receive priority for any needed transplant if that individual agrees that his or her organs will be available to other members of the insurance pool in the event of his or her death. … The main purpose [of this proposal] is to increase the supply of transplantable organs in order to save or improve more lives." Technical advances allows the use of donors that were previously rejected. For example, hepatitis C can be knowingly transplanted and treated in the organ recipient.In hospitals, organ network representatives routinely screen patient records to identify potential donors shortly in advance of their deaths. In many cases, organ-procurement representatives will request screening tests (such as blood typing) or organ-preserving drugs (such as blood pressure drugs) to keep potential donors organs viable until their suitability for transplants can be determined and family consent (if needed) can be obtained. This practice increases transplant efficiency, as potential donors who are unsuitable due to infection or other causes are removed from consideration before their deaths, and decreases the avoidable loss of organs. It may also benefit families indirectly, as the families of unsuitable donors are not approached to discuss organ donation. Distribution
The United States has two agencies that govern organ procurement and distribution within the country.
Hence, patients with a history of Fuchs dystrophy may be at a greater risk of corneal edema after ocular surgery as they have fewer functioning endothelial cells.FECD is classified into 4 stages, from early signs of guttae formation to end-stage subepithelial scarring. Diagnosis is made by biomicroscopic examination in the clinic. Other modalities, such as corneal thickness measurement (pachymetry), in-vivo confocal biomicroscopy, and specular microscopy can be used in conjunction.The exact pathogenesis is unknown but factors include endothelial cell apoptosis, sex hormones, inflammation, and aqueous humor flow and composition. Mutations in collagen VIII, a major component of Descemets membrane secreted by endothelial cells, have been linked to the early-onset FECD.As a genetically heterogeneous disease, the phenotype, or clinical experience of patients with Fuchs dystrophy may reflect the combination of genetic contributors to the disease. Some genetic lesions correlate with more severe disease and earlier onset. Therefore, some individuals may experience symptoms of the disease at a much earlier age, while others may not experience symptoms until late in life.Genes include:

Diagnosis
The diagnosis of Fuchs dystrophy is often made with slit lamp biomicroscopy. With direct illumination, the clinician can visualize guttae, the characteristic pathological changes in disease.Scheimpflug imaging, anterior segment optical coherence tomography, confocal microscopy, and specular microscopy are additional imaging techniques that can identify the presence of guttae and quantify the thickness of the cornea.