Kidney failure and transplant
The body sometimes recognizes a kidney transplant as a foreign object and try to protect the body by attacking it. In this regard, immunosuppressants are used to try and curb this. The medicines weaken the immune system. However, some patients will, in one way or another experience an episode of rejection. The body in this state is prone to infection due to the decreased strength of the immune system. These episodes of rejection don’t necessarily lead to losing a kidney or kidney failure. Mostly, rejections occur within the first six months after the transplant (Kidney Transplant Rejection 2020). The rejections are also mostly mild and only need adjustments to the medication. The probability of the body rejecting the transplant will decrease over time. Some of the symptoms of rejection are: Flu-like symptoms, fever of 101° F and above, reduced urine, gaining weight, pain and fatigue (Kidney Transplant Rejection 2020). However, most scenarios don’t show symptoms but are spotted through routine bloodwork.
There are a few reasons on what might have caused the symptoms for the 34-year-old male. The medication he took may have caused the symptoms. Prograf and Neoral can have side effects of abnormal kidney function, which could entail decreased urine output (Transplant Patient Education 2016).
Kidney failure has been mainly due to a defect in single-gene (Hildebrandt, 2010). Genes that cause the acute kidney rejection are; Enothelial cell growth factor (platelet‐derived), D component of complement (adipsin), Allograft inflammatory factor, HLA‐G histocompatibility antigen (class I, G), Rho‐specific guanine nucleotide exchange factor p114, Lysosomal‐associated multispanning membrane protein‐5, Signal transducer and activator of transcription(1, 91 kDa), Interleukin 10 receptor (alpha), Benzodiazapine receptor (peripheral), Src‐like‐adaptor, Ubiquitin‐conjugating enzyme E2L 6, ATP‐binding cassette (sub‐family C (CFTR/MRP), member 2), ATP‐binding cassette, sub‐family C (CFTR/MRP) (member 2), Integrin, beta 2 (antigen CD18 (p95)( lymphocyte) (function‐associated antigen 1; macrophage antigen 1 (mac‐1) beta subunit), Human serum albumin (ALB) gene and Lymphocyte‐specific protein tyrosine kinase (Flechner et al., 2004). The difference in immunosuppressive therapy, patients’ populations, and degrees of rejection play a role to reduce the genes identified above.
The immunosuppressive process involves using a triple therapy that consists of a calcineurin inhibitor, an adjunctive agent and corticosteroids. The T cells are responsible for “maintaining the immune response and limiting antigraft immunity” (Muntean & Lucan, 2013). Polyclonal antibodies are directed against the T-cell. Muromonab is an antibody that is produced by a combination of murine antibody-secreting B lymphocytes and nonsecreting myeloma cell line. This antibody reacts with the T-cell by holding CD3 and removing it from circulation. When the T-cell is back, it is with a devoid of CD3 (Muntean & Lucan, 2013). Alemtuzumab (Campath 1H) is another antibody that is used to minimize maintenance of immunosuppressive protocols. Humanized anti-CD25 are antibodies that work against the IL-2 receptors and in turn, prevent the acute rejection. Rituximab is an antibody that targets the CD20-antigen. It is used to avoid or reduce the formation of antibody hence treating acute rejection. Intravenous immune globulins prevent anti-HLA antibodies. These antibodies also suppress anti-HLA reactive T cells and B cell (Muntean & Lucan, 2013).