Mr. J.R. is a 73-year-old man, who was admitted to the hospital with clinical manifestations of gastroenteritis and possible renal injury. The patient’s chief complaints are fever, nausea with vomiting and diarrhea for 48 hours, weakness, dizziness, and a bothersome metallic taste in the mouth. The patient is pale and sweaty. He had been well until two days ago, when he began to experience severe nausea several hours after eating two burritos for supper. The burritos had been ordered from a local fast-food restaurant. The nausea persisted and he vomited twice with some relief. As the evening progressed, he continued to feel “very bad” and took some Pepto-Bismol to help settle his stomach. Soon thereafter, he began to feel achy and warm. His temperature at the time was 100. 5°F. He has continued to experience nausea, vomiting, and a fever. He has not been able to tolerate any solid foods or liquids. Since yesterday, he has had 5–6 watery bowel movements. He has not noticed any blood in the stools. His wife brought him to the ER because he was becoming weak and dizzy when he tried to stand up. His wife denies any recent travel, use of antibiotics, laxatives, or excessive caffeine, or that her husband has an eating disorder.
Case Study Questions
- The attending physician is thinking that Mr. J.R. has developed an Acute Kidney Injury (AKI). Analyzing the case presented name the possible types of Acute Kidney Injury. Link the clinical manifestations described to the different types of Acute Kidney injury.
- Create a list of risk factors the patient might have and explain why.
- Unfortunately, the damage on J.R. kidney became irreversible and he is now diagnosed with Chronic kidney disease. Please describe the complications that the patient might have on his Hematologic system (Coagulopathy and Anemia) and the pathophysiologic mechanisms involved.
- Your initial post should be at least 500 words per case study, formatted and cited in current APA style with support from at least 2 academic sources.
Possible types of Acute Kidney Injury (AKI) in the case of Mr. J.R. include:
- Prerenal AKI: Prerenal AKI occurs when there is a decrease in blood flow to the kidneys, leading to decreased perfusion and subsequent kidney damage. In this case, Mr. J.R.’s symptoms of weakness, dizziness, and pale, sweaty appearance could be indicative of prerenal AKI. The presence of gastroenteritis with dehydration due to vomiting and diarrhea may have resulted in reduced blood volume and perfusion to the kidneys, leading to prerenal AKI.
- Intrinsic AKI: Intrinsic AKI involves direct damage to the kidney tissue. It can be further classified into different subtypes, including acute tubular necrosis (ATN), acute interstitial nephritis (AIN), and glomerulonephritis. Considering the patient’s symptoms and history, ATN seems to be a potential cause. ATN can occur as a result of ischemia (reduced blood flow) to the kidneys, which may be associated with dehydration and decreased renal perfusion due to gastroenteritis.
- Postrenal AKI: Postrenal AKI is caused by obstruction of the urinary tract, which prevents the normal flow of urine from the kidneys. Although the case study does not provide specific information about urinary symptoms or obstruction, it is still worth considering as a possible cause. However, the absence of any urinary symptoms or history of urinary tract obstruction makes postrenal AKI less likely in this case.
Potential risk factors for Mr. J.R. include:
- Advanced age: Mr. J.R. is 73 years old, and advanced age is a well-known risk factor for the development of AKI. With age, the kidneys undergo structural and functional changes, making them more vulnerable to injury.
- Dehydration: The patient’s symptoms of nausea, vomiting, and diarrhea for 48 hours suggest significant fluid loss, which can lead to dehydration. Dehydration reduces blood volume and subsequently decreases renal perfusion, increasing the risk of AKI.
- Use of medications: Although the case study does not mention any medication use, certain medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and some antibiotics can cause or contribute to AKI. However, the absence of a history of medication use makes this less likely in this case.
- Gastroenteritis: Gastroenteritis, characterized by inflammation of the gastrointestinal tract, can lead to AKI. The combination of vomiting, diarrhea, and subsequent dehydration in Mr. J.R. suggests that gastroenteritis might be a contributing factor.
- Possible exposure to toxins: The case mentions the consumption of burritos from a local fast-food restaurant, which raises the possibility of foodborne toxins or bacterial contamination. Certain toxins, such as those produced by E. coli or other bacteria, can cause AKI.
Complications on the Hematologic system in Chronic Kidney Disease (CKD) include coagulopathy and anemia. The pathophysiologic mechanisms involved are as follows:
- Coagulopathy: In CKD, there is a disruption in the normal balance between procoagulant and anticoagulant factors, leading to a prothrombotic state. Several factors contribute to coagulopathy in CKD, including decreased synthesis of clotting factors (e.g., fibrinogen), impaired platelet function, and increased levels of procoagulant proteins (e.g., von Willebrand factor). These abnormalities can lead to an increased risk of thrombotic events, such as deep vein thrombosis (DVT) or pulmonary embolism.
- Anemia: Anemia is a common complication of CKD. The kidneys play a crucial role in the production of erythropoietin (EPO), a hormone that stimulates red blood cell production in the bone marrow. In CKD, the kidneys are unable to produce sufficient EPO, resulting in decreased red blood cell production and subsequent anemia. Anemia in CKD is further aggravated by factors such as iron deficiency, shortened red blood cell lifespan, and inflammation-induced inhibition of erythropoiesis.
Both coagulopathy and anemia in CKD can contribute to an increased risk of complications such as cardiovascular events, reduced quality of life, and increased morbidity and mortality. Timely management of these hematologic complications, including correction of anemia with erythropoiesis-stimulating agents and iron supplementation, and appropriate anticoagulation strategies, is crucial in the management of CKD patients.
References:
- Ronco, C., Bellomo, R., & Kellum, J. A. (Eds.). (2018). Acute kidney injury. CRC Press.
- Locatelli, F., Nissenson, A. R., & Barrett, B. J. (2018). Long-term follow-up in kidney disease patients: from observational studies to clinical trials. Kidney international supplements, 8(1), 21-27.