Bile Cast Nephropathy (Cholemic Nephropathy) Associated with Hepatitis A-Induced Acute Liver Failure and Haemolysis in a Patient with Glucose-6-Phosphate Dehydrogenase Deficiency.

Q3 Medicine European journal of case reports in internal medicine Pub Date : 2025-01-27 eCollection Date: 2025-01-01 DOI:10.12890/2025_005064
Ali Hamdan, Johny Salem, Karam Karam, Maria Ziadeh, Pierre Hani
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Abstract

Introduction: The hepatitis A virus (HAV) is a common cause of acute hepatitis, while glucose-6-phosphate dehydrogenase (G6PD) deficiency is a widespread enzyme disorder that predisposes individuals to haemolysis and hyperbilirubinemia. We report a case of a G6PD-deficient patient with hepatitis A-induced acute renal failure (ARF), highlighting the role of plasmapheresis and haemodialysis in management.

Case description: A 40-year-old male with G6PD deficiency and hypertension was transferred for further care after presenting with fever, diarrhoea and jaundice. Laboratory results showed severe haemolysis and elevated bilirubin (70 μmol/l); hepatitis A serology was positive. The patient developed acute liver failure and ARF, with creatinine reaching 7.3 mg/dl. Plasmapheresis and haemodialysis were initiated, leading to stabilisation of renal function and a significant decrease in bilirubin by six weeks post-discharge.

Discussion: G6PD deficiency increases the risk of haemolysis, especially during infections such as hepatitis A. This can lead to severe hyperbilirubinemia and complications including bile cast nephropathy. In this case, plasmapheresis effectively reduced bilirubin and inflammatory mediators, while haemodialysis addressed renal dysfunction. Together, these therapies were crucial in stabilising renal function.

Conclusion: Bile cast nephropathy is an important cause of kidney injury in severe hyperbilirubinemia. This case highlights the effectiveness of plasmapheresis and haemodialysis in managing the condition and supporting renal recovery, especially in the absence of established treatment guidelines.

Learning points: Bile cast nephropathy is a significant yet underrecognised cause of acute kidney injury, often associated with severe hyperbilirubinemia in the setting of acute liver failure.In this case, glucose-6-phosphate dehydrogenase (G6PD) deficiency combined with hepatitis A-induced haemolysis led to elevated bilirubin levels, contributing to kidney injury.This case highlights the importance of extracorporeal therapies in managing bile cast nephropathy and promoting renal function recovery, particularly in the absence of standard treatment guidelines.

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6-磷酸葡萄糖脱氢酶缺乏症患者胆铸型肾病(胆碱性肾病)与甲型肝炎诱导的急性肝衰竭和溶血相关
甲型肝炎病毒(HAV)是急性肝炎的常见病因,而葡萄糖-6-磷酸脱氢酶(G6PD)缺乏症是一种广泛存在的酶紊乱,易导致个体溶血和高胆红素血症。我们报告一例g6pd缺陷患者合并甲型肝炎引起的急性肾功能衰竭(ARF),强调血浆置换和血液透析在治疗中的作用。病例描述:一名患有G6PD缺乏症和高血压的40岁男性在出现发烧、腹泻和黄疸后被转送进一步治疗。实验室结果:严重溶血,胆红素升高(70 μmol/l);甲肝血清学阳性。患者出现急性肝功能衰竭和ARF,肌酐达到7.3 mg/dl。开始血浆置换和血液透析,导致肾功能稳定,并在出院后6周显著降低胆红素。讨论:G6PD缺乏增加溶血的风险,特别是在感染如甲型肝炎时,这可导致严重的高胆红素血症和并发症,包括胆汁铸型肾病。在这种情况下,血浆置换有效地降低了胆红素和炎症介质,而血液透析则解决了肾功能障碍。总之,这些疗法对稳定肾功能至关重要。结论:胆汁铸型肾病是严重高胆红素血症肾损伤的重要原因。该病例强调了血浆置换和血液透析在控制病情和支持肾脏恢复方面的有效性,特别是在缺乏既定治疗指南的情况下。学习要点:胆汁型肾病是急性肾损伤的重要原因,但尚未得到充分认识,通常与急性肝功能衰竭时严重的高胆红素血症相关。在这种情况下,葡萄糖-6-磷酸脱氢酶(G6PD)缺乏合并甲型肝炎诱导的溶血导致胆红素水平升高,导致肾损伤。本病例强调了体外治疗在管理胆汁投射肾病和促进肾功能恢复中的重要性,特别是在缺乏标准治疗指南的情况下。
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来源期刊
CiteScore
2.10
自引率
0.00%
发文量
166
审稿时长
8 weeks
期刊介绍: The European Journal of Case Reports in Internal Medicine is an official journal of the European Federation of Internal Medicine (EFIM), representing 35 national societies from 33 European countries. The Journal''s mission is to promote the best medical practice and innovation in the field of acute and general medicine. It also provides a forum for internal medicine doctors where they can share new approaches with the aim of improving diagnostic and clinical skills in this field. EJCRIM welcomes high-quality case reports describing unusual or complex cases that an internist may encounter in everyday practice. The cases should either demonstrate the appropriateness of a diagnostic/therapeutic approach, describe a new procedure or maneuver, or show unusual manifestations of a disease or unexpected reactions. The Journal only accepts and publishes those case reports whose learning points provide new insight and/or contribute to advancing medical knowledge both in terms of diagnostics and therapeutic approaches. Case reports of medical errors, therefore, are also welcome as long as they provide innovative measures on how to prevent them in the current practice (Instructive Errors). The Journal may also consider brief and reasoned reports on issues relevant to the practice of Internal Medicine, as well as Abstracts submitted to the scientific meetings of acknowledged medical societies.
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