NURS 6501N Week 1 Assignment MD1 WLD

The case study that I will be analyzing involves a 34-year-old Hispanic-American male with end-stage renal disease who received a kidney transplant from a cadaver donor, due to no family member match. His postoperative was uneventful, and he was discharged with the antirejection drugs: Tacrolimus, Cyclosporine, and Imuran. He did well and returned to his job as a policeman after three months. Six months after the transplant, he began to gain weight, have lOMoARcPSD| 2 decreased urine output, fatigued, and began having elevated temperatures up to 101˚F. He was evaluated by his nephrologist and was diagnosed with acute kidney transplant rejection. The purpose of this paper is to describe the cellular, genes, and mechanisms of the immunity process of acute kidney transplant rejection. Why the patient presented the symptoms described? The symptoms that he is experiencing are caused by his body’s rejection of the kidney transplant and the side effects of the antirejection medication, the immunosuppressant prescribed Tacrolimus. Tacrolimus is reported to cause serious side effects, such as decreased urination, weight gain, and tiredness (Tacrolimus: MedlinePlus Drug Information, n.d.). The elevated temperatures are a result of the body’s inflammatory response to decreased urine output from the kidney not functioning properly, and unable to filter out the toxins from the body. Genes that may be associated with the development of the disease Acute rejection is a cell-mediated immune response that occurs within days to months after transplantation (McCance & Huether, 2019). Acute kidney transplant rejection develops from the Major histocompatibility complex (MHC) class I and class II genes the human leukocyte antigen (HLA). The genes and cells of the transplanted kidney from the donor have different genes and HLAs than the recipient. When this occurs, the body will respond by building an immune response to the foreign HLAs antigens. This then causes the recipient’s lymphocytes to interact with the donor’s dendritic cells within the transplanted organ tissue, which results in the recipient’s TH1 and TC cells going against the donor’s antigens (McCance & Huether, 2019). The TH1 cells then release cytokines that then activate macrophages and the TC cells directly attack the endothelial cells in the transplanted tissue resulting in acute rejection of the kidney (McCance & Huether, 2019).