{"title":"The most lethal human protozoan parasite is plasmodium falciparum: severe malaria-associated acute renal failure - a case report.","authors":"Gudisa Bereda","doi":"10.1097/MS9.0000000000000988","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction and importance: </strong>Malaria continues to be a significant global public health problem, particularly in endemic nations. The most common cause of acute renal failure is a <i>Plasmodium falciparum</i> infection.</p><p><strong>Case presentation: </strong>A 28-year-old male was brought into the emergency room with significant complaints of fatigue, chills, fever, and a lack of appetite. The patient had no prior history of malaria. He was not given any antimalarial medication as prophylaxis while traveling to his workplace. As a result of laboratory investigations to identify malarial parasites in peripheral blood using thin and thick smears, malaria parasites were found in the patient's blood. At the border of the colitis, the liver was palpable. Both the chest radiograph and abdominal ultrasonography were clear. His level of consciousness assessment indicated a Glasgow coma scale reading of 10 out of 15. He received 1000 ml of normal saline solution with 40% glucose solution as part of his supportive care. He received intravenous artesunate 60 mg (2.4 mg/kg) when he was admitted to an ICU, and then every 12 and 24 h for the next 3 days (a total of three doses, 540 mg).</p><p><strong>Clinical discussion: </strong>A typical symptom of severe malaria is acute kidney injury, which also carries its own risk of death. In regions with active transmission, <i>Plasmodium falciparum</i> is recognized as a significant contributor to acute renal damage.</p><p><strong>Conclusion: </strong>The mechanism proposed for kidney injury by severe malaria is hemodynamic dysfunction, followed by inflammation and immunological dysregulation in the patient in this study. He had reduced serum sodium levels within the red blood cells, which led to calcium influx into the cell, altering the red blood cell's deformability.</p>","PeriodicalId":8025,"journal":{"name":"Annals of Medicine and Surgery","volume":"86 12","pages":"7314-7317"},"PeriodicalIF":1.7000,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11623832/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of Medicine and Surgery","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1097/MS9.0000000000000988","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/12/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction and importance: Malaria continues to be a significant global public health problem, particularly in endemic nations. The most common cause of acute renal failure is a Plasmodium falciparum infection.
Case presentation: A 28-year-old male was brought into the emergency room with significant complaints of fatigue, chills, fever, and a lack of appetite. The patient had no prior history of malaria. He was not given any antimalarial medication as prophylaxis while traveling to his workplace. As a result of laboratory investigations to identify malarial parasites in peripheral blood using thin and thick smears, malaria parasites were found in the patient's blood. At the border of the colitis, the liver was palpable. Both the chest radiograph and abdominal ultrasonography were clear. His level of consciousness assessment indicated a Glasgow coma scale reading of 10 out of 15. He received 1000 ml of normal saline solution with 40% glucose solution as part of his supportive care. He received intravenous artesunate 60 mg (2.4 mg/kg) when he was admitted to an ICU, and then every 12 and 24 h for the next 3 days (a total of three doses, 540 mg).
Clinical discussion: A typical symptom of severe malaria is acute kidney injury, which also carries its own risk of death. In regions with active transmission, Plasmodium falciparum is recognized as a significant contributor to acute renal damage.
Conclusion: The mechanism proposed for kidney injury by severe malaria is hemodynamic dysfunction, followed by inflammation and immunological dysregulation in the patient in this study. He had reduced serum sodium levels within the red blood cells, which led to calcium influx into the cell, altering the red blood cell's deformability.