A major point of contention is whether transplantation should be allowed at all if the patient is not yet fully biologically dead, and if brain death is acceptable, whether the persons whole brain needs to have died, or if the death of a certain part of the brain is enough for legal and ethical and moral purposes. Most organ donation for organ transplantation is done in the setting of brain death. However, in Japan this is a fraught point, and prospective donors may designate either brain death or cardiac death – see organ transplantation in Japan. In some nations such as Belgium, France, Netherlands, New Zealand, Poland, Portugal, Singapore and Spain, everyone is automatically an organ donor unless they opt out of the system. Elsewhere, consent from family members or next-of-kin is required for organ donation. The non-living donor is kept on ventilator support until the organs have been surgically removed. If a brain-dead individual is not an organ donor, ventilator and drug support is discontinued and cardiac death is allowed to occur. In the United States, where since the 1980s the Uniform Determination of Death Act has defined death as the irreversible cessation of the function of either the brain or the heart and lungs, the 21st century has seen an order-of-magnitude increase of donation following cardiac death. In 1995, only one out of 100 dead donors in the nation gave their organs following the declaration of cardiac death.
The most common ones are factor V Leiden (a mutation in the F5 gene at position 1691) and prothrombin G20210A, a mutation in prothrombin (at position 20210 in the 3 untranslated region of the gene).The rare forms of congenital thrombophilia are typically caused by a deficiency of natural anticoagulants. They are classified as "type I" and are more severe in their propensity to cause thrombosis. The main ones are antithrombin III deficiency, protein C deficiency and protein S deficiency. Milder rare congenital thrombophilias are factor XIII mutation and familial dysfibrinogenemia (an abnormal fibrinogen). It is unclear whether congenital disorders of fibrinolysis (the system that destroys clots) are major contributors to thrombosis risk. Congenital deficiency of plasminogen, for instance, mainly causes eye symptoms and sometimes problems in other organs, but the link with thrombosis has been more uncertain.Blood group determines thrombosis risk to a significant extent. Those with blood groups other than type O are at a 2- to 4-fold relative risk. O blood group is associated with reduced levels of von Willebrand factor – because of increased clearance – and factor VIII, which is related to thrombotic risk . Acquired
A number of acquired conditions augment the risk of thrombosis. A prominent example is antiphospholipid syndrome, which is caused by antibodies against constituents of the cell membrane, particularly lupus anticoagulant (first found in people with the disease systemic lupus erythematosus but often detected in people without the disease), anti-cardiolipin antibodies, and anti-β2-glycoprotein 1 antibodies; it is therefore regarded as an autoimmune disease.