NURS-6501 Week 2 Case Study Analysis

NURS-6501 Week 2 Case Study Analysis

Altered Physiology

Question 1

The patient displayed symptoms consistent with acute kidney rejection, a severe complication following kidney transplantation. Patients who undergo renal transplant are vulnerable to acute kidney rejection due to the immunosuppression required post-transplantation (Lai et al., 2021). Proper monitoring by the patient’s nephrologist in the initial months after transplantation, with medication adjustments as needed, is crucial.

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The patient also exhibited weight gain, a common occurrence in rejection cases. Excessive weight gain can hinder the patient’s tolerance to the anti-rejection drug Cyclosporine (Neoral), potentially causing toxicity and life-threatening consequences if left untreated (Lai et al., 2021). Reduced urine output and elevated body temperature were also noted, indicating inflammation. If left unaddressed, severe inflammation can lead to organ damage.

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Furthermore, the patient’s symptoms align with acute kidney rejection, particularly because he received a kidney from a cadaveric donor. While some degree of organ rejection is expected, it can be managed using medications like cyclosporine and tacrolimus (Justiz Vaillant et al., 2022). However, in this case, the patient couldn’t tolerate the combination of these drugs, leading to rejection symptoms.

Question 2

The genes most likely associated with the development of acute kidney transplant rejection are the HLA genes and the B7-H1 gene. HLA genes, located on chromosome 6 and designated as HLA-A, -B, -C, -DRB1, -DQB1, -DQA1, -DPB1, and -DQA2, play a crucial role in determining transplant compatibility (Brehm et al., 2019).

HLA-DRB1*15:01 stands out as a significant risk factor for acute kidney transplant rejection in cases involving allogeneic transplantation from an HLA-DRB1*15:01 donor with graft-versus-host disease (GVHD) (Brehm et al., 2019). Studies suggest that this gene contributes to 10%-45% of acute kidney transplant rejection cases following allogeneic transplantation. HLA-DQA1*02:01 is another gene that increases the risk of acute kidney transplant rejection, especially when the recipient receives a graft from an identical HLA-DQA1*02:01 genetic match (Loupy & Lefaucheur, 2018).

The patient’s genetic makeup likely plays a significant role in the development of acute kidney transplant rejection (Lai et al., 2021). The presence of HLA-DR2 in the transplanted kidney increases the likelihood of a robust immune response, potentially leading to inflammation and upregulation of pro-inflammatory genes.

Question 3

Immunosuppression involves weakening the immune system, rendering an individual more susceptible to illnesses (McCance & Huether, 2019). The immune system comprises white blood cells responsible for defending the body against pathogens like bacteria and viruses. These cells produce antibodies that bind to foreign invaders.

Several factors, including medications, infections, and cancer therapies, can induce immunosuppression. Cancer therapies (chemotherapy) and organ transplantation are the primary culprits behind immunosuppression (McCance & Huether, 2019). Additionally, individuals with HIV/AIDS undergoing antiretroviral therapy (ART) experience immunosuppression, preventing them from effectively combating infections.

Cancer therapies and organ transplantation weaken the immune system by either destroying specific components or suppressing their function, making it less capable of fighting infections or preventing tumor growth (McCance & Huether, 2019). Immunosuppressive drugs are employed to prevent organ and tissue rejection following transplant surgeries, as well as after bone marrow transplants.

In this case study, the patient’s immunosuppression was initiated with Tacrolimus (Prograf), Cyclosporine (Neoral), and Imuran (Azathioprine). These drugs fall under the category of TAC-susceptible triazines (TACS), functioning by inhibiting T-cells, a component of the immune system (McCance & Huether, 2019). This inhibition prevents T-cells from reacting to transplanted organs or tissues.

Immunosuppression exerts various effects on the body:

– It reduces inflammation, mitigating the risk of organ damage.
– It diminishes the activity of white blood cells, bolstering infection prevention and aiding in healing.
– It curtails the production of pain and fever-inducing substances, facilitating the treatment of pain and illnesses related to rejection or inflammation.

References

Brehm, M. A., Kenney, L. L., Wiles, M. V., Low, B. E., Tisch, R. M., Burzenski, L., Mueller, C., Greiner, D. L., & Shultz, L. D. (2019). Lack of acute xenogeneic graft-versus-host disease, but retention of T-cell function following engraftment of human peripheral blood mononuclear cells in NSG mice deficient in MHC class I and II expression. FASEB journal: official publication of the Federation of American Societies for Experimental Biology, 33(3), 3137–3151. https://doi.org/10.1096/fj.201800636R

Justiz Vaillant, A. A., Vashisht, R., & Zito, P. M. (2022). Immediate Hypersensitivity Reactions. In StatPearls. StatPearls Publishing.

Lai, X., Zheng, X., Mathew, J. M., Gallon, L., Leventhal, J. R., & Zhang, Z. J. (2021). Tackling Chronic Kidney Transplant Rejection: Challenges and Promises. Frontiers in immunology, 12, 661643. https://doi.org/10.3389/fimmu.2021.661643

Loupy, A., & Lefaucheur, C. (2018). Antibody-Mediated Rejection of Solid-Organ Allografts.

Altered Physiology

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