The Acute Kidney Injury (AKI) Research
The patient under consideration has allegedly developed an Acute Kidney Injury (AKI). However, this disease implies specific types that differ in symptoms and treatment. It leads to the necessity to review the possible types and compare the patient’s information with their specificities. The variations of AKI include pre-renal AKI, acute post-renal obstructive nephropathy, and intrinsic acute kidney diseases (Makris & Spanou, 2016). The first type is the actual disease since the last two represent the consequences of other health conditions that can evolve into pre-renal AKI (Makris & Spanou, 2016). Hence, the task is to define the patient’s current state and its correspondence to one of the specified types.
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The history of Mr. J.R. proves that the nature of his condition is purely intrinsic. It allows excluding acute post-renal obstructive nephropathy from the list. The patient’s symptoms include nausea, diarrhea, and vomiting typical for the condition (Makris & Spanou, 2016). They correspond to the clinical manifestations of both intrinsic AKI types and, therefore, require individual consideration. Thus, the analysis will allow identifying the presence of either pre-renal AKI or intrinsic acute kidney diseases. The patient’s current health condition implies the presence of specific risks, and they should also be considered while deciding on his treatment. Such a disease as an Acute Kidney Injury (AKI) tends to occur in connection with other health issues or the emergence of new health issues (“Acute kidney failure,” n.d.). In the case of Mr. J.R., the principal consideration is his advanced age that indicates a higher probability of acute kidney failure (“Acute kidney failure,” n.d.). Hence, the treatment of the patient should be performed while taking into account this factor. Other circumstances that might have an impact on possible complications include the risks of developing new diseases. As can be seen from the patient’s medical history, he did not use any antibiotics and did not have eating disorders before this event. Nevertheless, this information is not enough for making the ultimate decision on his treatment since the previous health conditions also influence the risks for complications (“Acute kidney failure,” n.d.). The most common factors affecting the emergence of AKI are blockages in the blood vessels, diabetes, high blood pressure, heart failure, and kidney and liver diseases (“Acute kidney failure,” n.d.). Therefore, they should be added to the consideration of the patient’s age. Since the diagnosis of the patient, which is chronic kidney disease, has been confirmed, and the damage is recognized as irreversible, it is vital to prevent further complications deriving from his health condition. They mostly relate to the change in his body caused by the improper functioning of kidneys that ensure the work of all human organs (“Complications of CKD,” n.d.). The impact of such complications on one’s hematologic system is reflected in the emergence of anemia due to the lack of red blood cells produced by kidneys (“Complications of CKD,” n.d.). Another issue resulting from chronic kidney disease is coagulopathy caused by blood clots (“Complications of CKD,” n.d.). These circumstances require constant medical assistance for the patient to prevent a negative outcome. The pathophysiologic mechanisms involved in the emergence of specified complications relate to abnormalities caused by chronic kidney disease. They include ischemia, inflammatory processes, vasoconstriction, and endothelial injury (Makris & Spanou, 2016). These consequences reflect the incorrect work of kidneys and the corresponding processes. The overall health condition resulting from the emergence of chronic kidney disease can be described with the inclusion of other complications and pathophysiology. References Acute kidney failure (n.d.). Mayo Clinic. 2020, Web.
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Complications of CKD (n.d.). American Kidney Fund. 2020, Web. Makris, K., & Spanou, L. (2016). Acute kidney injury: Definition, pathophysiology, and clinical phenotypes. The Clinical Biochemist Reviews, 37(2), 85-98.