Hyperacute rejection is caused by:
Hyperacute rejection, a very rapid type of rejection, results in irreversible damage and graft loss within minutes to hours after organ reperfusion. It is triggered by preformed antibodies against the donor's human leukocyte antigen (HLA) or ABO blood group antigens. These antibodies activate a series of events that result in diffuse intravascular coagulation, causing ischemic necrosis of the graft. Fortunately, pretransplant blood group typing and cross-matching (in which the donor's cells are mixed with the recipient's serum, and then destruction of the cells is observed) have virtually eliminated the incidence of hyperacute rejection.
The mechanism of action of azathioprine (AZA) is:
An antimetabolite, azathioprine (AZA) is converted to 6-mercaptopurine and inhibits both the de novo purine synthesis and salvage purine synthesis. AZA decreases T-lymphocyte activity and decreases antibody production. It has been used in transplant recipients for more than 40 years, but became an adjunctive agent after the introduction of cyclosporine. With the development of newer agents such as mycophenolate mofetil (MMF), the use of AZA has decreased significantly. However, it is preferred in recipients who are considering conceiving a child, because MMF is teratogenic in females and can cause birth defects. AZA might be an option for recipients who cannot tolerate the gastrointestinal (GI) side effects of MMF.
The most significant side effect of AZA, often dose-related, is bone marrow suppression. Leukopenia is often reversible with dose reduction or temporary cessation of the drug. Other significant side effects include hepatotoxicity, pancreatitis, neoplasia, anemia, and pulmonary fibrosis. Its most significant drug interaction is with allopurinol, which blocks AZJ's metabolism, increasing the risk of pancytopenia. Recommendations are to not use AZA and allopurinol together, or if doing so is unavoidable, to decrease the dose of AZA by 75%.
Which of the following is NOT a side effect of cyclosporine?
Side effects and drug interactions ofthe main immunosuppressive drugs:
ACE-I = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blocker; NSAID = nonsteroidal anti-infiammatory d rug; TMP-SMX = trimethoprim-sulfamethoxazole
Postrenal transplant graft thrombosis usually occurs:
One of the most devastating postoperative complications in kidney recipients is graft thrombosis. It is rare, occurring in fewer than 1% of recipients. The recipient risk factors include a history of recipient hypercoagulopathy and severe peripheral vascular disease; donor-related risk factors include the use of en bloc or pediatric donor kidneys, procurement damage, technical factors such as intimal dissection or torsion of vessels, and hyperacute rejection. Graft thrombosis usually occurs within the first several days posttransplant. Acute cessation of urine output in recipients with brittle posttransplant diuresis and the sudden onset of hematuria or graft pain should arouse suspicion of graft thrombosis. Doppler ultrasound may help confirm the diagnosis. In cases of graft thrombosis, an urgent thrombectomy is indicated; however, it rarely results in graft salvage.
The 1 -year graft survival after renal transplantation is:
According to the 20 10 Scientific Registry of Transplant Recipients (SRTR) annual report, a total of 84,614 adult patients were on the kidney transplant waiting list, including 33,2 15 added just that year. Yet in 2009, only 15,964 adult kidney transplants were performed in the United States (99 12 with a deceased donor and 6052 with a living donor). Of note, the number of patients added to the kidney transplant waiting list has increased every year, but the number ofkidney transplants performed has been declining since 2006. On the positive side, posttransplant outcomes have continued to improve: in 2009, the 1 -year graft survival rate with a living donor kidney was 96.5%; with a deceased donor kidney, the rate was 92.0%.
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