Module 1 Assignment: Case Study Analysis
Body functioning at the cellular level is influenced by genetic, environmental, and molecular among other factors. My assigned case for this week’s discussion is about a 38-year-old Hispanic American male who had a kidney transplant from cadaveric donation following end-stage renal disease (ESRD).
He is then discharged on Azathioprine, cyclosporine, and tacrolimus to prevent rejection. However, after six months, he presented with weight gain, fatigue, fever, and decreased urine output. The purpose of this discussion is to explain the pathophysiology of this patient’s presentation, the genetic basis of his disease, and the process of immunosuppression.
Weight gain, decreased urine output, fatigue, and fever are suggestive of acute kidney injury. However, other differentials such as acute transplant rejection, drug toxicity, vascular thrombosis, and thrombotic microangiopathy (Dudreuilh et al., 2018). On the readmission, the patient was diagnosed by his nephrologist with acute transplant rejection.
Acute transplant rejection is mediated by cell-mediated immunity, where host immune cells attack the allograft. In this case, the host immune cells attacked the new kidney (McCance & Huether, 2019). Unfortunately, that was the only functioning kidney he had, he developed acute kidney injury.
In acute kidney injury, waste and water excretion become limited with limited kidney function. Water retention leads to weight gain and reduced urine output. Retention of wastes such as urea led to uremia that presented as fatigue.
According to Dudreuilh et al. (2018), septic acute kidney injury is common in patients with acute kidney transplant rejection. This explains the cause of the patient’s fever. The immunosuppressive medications were responsible for the reduction in immune system function and opened the way for opportunistic infections.
Therefore, acute kidney due to or in conjunction with the medications, immunologic reactions, and bacterial infections could be responsible for the patient’s symptoms.
The patient is of Hispanic descent and presented at first with end-stage renal disease. ESRD is common among Hispanics and is usually associated with diabetes mellitus among this population (Desai et al., 2019). In this patient, acute kidney transplant rejection would result from various genes.
Reynolds (2019), through the National Institute of Health (NIH) research matters, raised concern about gene deletion that involved a gene called LIMS1 that could be responsible for kidney transplant rejection among patients and presented a higher risk – about 80%.
However, a recent study by Bogacz et al. (2021) established that the impact of polymorphisms in TGFB1 and CTLA4 genes were not responsible for the rejection of kidney transplants. Kang et al. (2021) found out that rejection could be a result of HLA-G 14-bp insertion/deletion polymorphism in some individuals, especially among Asians.
Immunosuppression reduces the body’s capacity to react to foreign antigens, objects, or organs. Immunosuppression enhances the proliferation of fibroblasts and the synthesis of matrix elements. Therefore, it subverts the surveillance by innate and adaptive immunity against these foreign organs and organisms (Huaux, 2018).
Some medications suppress the bone marrow’s ability to make new cells to help in the immunologic fight. This negatively impacts other systems that rely on these cells and the mediators they produce. The hematologic system is rendered weak, and resistant anemia would lead to hypoperfusion of end organs.
The patient developed acute rejection and presented with features of septic acute kidney injury as a result of water and waste retentions with possible superimposed infection. Acute kidney due to or in conjunction with the medications, immunologic reactions, and bacterial infections could be responsible for his symptoms. LIMS1 deletion and HLA-G 14-bp insertion/deletion polymorphism could have increased his susceptibility to his rejection. The immunosuppressive medications used limited his innate and adaptive defense systems leading to reduced cell prediction and possible anemia.
Bogacz, A., Wolek, M., Sieńko, J., Czerny, B., Machaliński, B., Olbromski, P., & Kotowski, M. (2021). Influence of TGFB1 and CTLA4 polymorphisms on calcineurin inhibitors dose and risk of acute rejection in renal transplantation. Scientific Reports, 11(1), 17531. https://doi.org/10.1038/s41598-021-96457-7
Desai, N., Lora, C. M., Lash, J. P., & Ricardo, A. C. (2019). CKD and ESRD in US Hispanics. American Journal of Kidney Diseases: The Official Journal of the National Kidney Foundation, 73(1), 102–111. https://doi.org/10.1053/j.ajkd.2018.02.354
Dudreuilh, C., Aguiar, R., & Ostermann, M. (2018). Acute kidney injury in kidney transplant patients. Acute Medicine, 17(1), 31–35. https://pubmed.ncbi.nlm.nih.gov/29589603/
Huaux, F. (2018). The emerging role of immunosuppression in diseases induced by micro-and nano-particles: Time to revisit the exclusive inflammatory scenario. Frontiers in Immunology, 9, 2364. https://doi.org/10.3389/fimmu.2018.02364
Kang, S. W., Oh, E., Cho, W., Kim, M., Park, E. J., Kwack, K. H., Chung, K., Nam, O. H., Chae, Y. K., & Ban, J. Y. (2021). HLA-G 14bp Ins/Del polymorphism in the 3′UTR region and acute rejection in kidney transplant recipients: An updated meta-analysis. Medicine (Kaunas, Lithuania), 57(10), 1007. https://doi.org/10.3390/medicina57101007
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (9th ed.). Mosby.
Reynolds, S. (2019). Gene deletion raises the risk of kidney transplant rejection. NIH Research Matters. https://www.nih.gov/news-events/nih-research-matters/gene-deletion-raises-risk-kidney-transplant-rejection