Srour Fawzi, Pourcelet Aline, Beklevic Ishak, Benoit Guillaume, de Grandsaigne Serge Treille, Neveux Nathan
Department of Internal Medicine, Medical School ULB, Brussels, Belgium.
Department of Nephrology, University Hospital Marie-Curie, Charleroi, Belgium.
Eur J Case Rep Intern Med. 2025 Jul 23;12(8):005661. doi: 10.12890/2025_005661. eCollection 2025.
INTRODUCTION: Bile cast nephropathy (BCN) is a rare and often overlooked cause of acute kidney injury (AKI), usually seen in the context of severe hyperbilirubinemia. It results from the deposition of bile pigments and bile casts in renal tubules, specifically distal and collector tubules, leading to obstruction and direct tubular toxicity. CASE DESCRIPTION: We describe the case of 49-year-old male who presented with severe jaundice and oliguric AKI. With the gradual resolution of liver dysfunction, the patient's kidney function also improved. However, during the recovery phase, the patient developed persistent hypokalaemia and normal anion gap metabolic acidosis. Further work-up was consistent with distal renal tubular acidosis (dRTA). DISCUSSION: While BCN is being increasingly recognized in patients with cholestatic liver diseases, complications arising during the recovery phase - particularly acid-base disturbances like dRTA - are rarely reported. In this case, the onset of dRTA during renal recovery may reflect delayed or selective tubular healing after bile-induced injury. This case highlights the importance of continued monitoring for renal tubular defects even after apparent improvement in glomerular function. CONCLUSION: This case emphasizes the need to consider dRTA as a potential complication in patients recovering from BCN. Close follow-up of electrolyte and acid-base parameters is advised during renal recovery, especially in the presence of persistent hypokalaemia. LEARNING POINTS: Bile cast nephropathy (BCN) is an under-recognized cause of acute kidney injury (AKI) in patients with severe hyperbilirubinemia and should be considered in the differential diagnosis of AKI in jaundiced patients.Distal renal tubular acidosis (dRTA) can emerge during the recovery phase of BCN-related AKI, possibly due to tubular dysfunction from bile-induced injury, highlighting the need for close metabolic monitoring after renal recovery.The co-occurrence of BCN and dRTA emphasizes the importance of serial electrolyte assessments and acid-base evaluation in jaundiced patients with AKI, even after apparent improvement in renal function.
引言：胆汁管型肾病（BCN）是急性肾损伤（AKI）的一种罕见且常被忽视的病因，通常见于严重高胆红素血症的情况下。它是由胆色素和胆汁管型在肾小管，特别是远端小管和集合小管中的沉积导致的，从而引起梗阻和直接的肾小管毒性。 病例描述：我们描述了一名49岁男性患者，他出现严重黄疸和少尿性AKI。随着肝功能逐渐恢复，患者的肾功能也有所改善。然而，在恢复阶段，患者出现了持续性低钾血症和正常阴离子间隙代谢性酸中毒。进一步检查与远端肾小管酸中毒（dRTA）相符。 讨论：虽然胆汁淤积性肝病患者中BCN越来越受到认可，但恢复阶段出现的并发症——特别是像dRTA这样的酸碱紊乱——鲜有报道。在本病例中，肾恢复过程中dRTA的发生可能反映了胆汁诱导损伤后肾小管愈合延迟或选择性愈合。该病例强调了即使肾小球功能明显改善后，持续监测肾小管缺陷的重要性。 结论：本病例强调了在BCN恢复患者中考虑dRTA作为潜在并发症的必要性。建议在肾恢复期间密切随访电解质和酸碱参数，尤其是存在持续性低钾血症时。 学习要点：胆汁管型肾病（BCN）是严重高胆红素血症患者急性肾损伤（AKI）的一种未被充分认识的病因，在黄疸患者AKI的鉴别诊断中应予以考虑。远端肾小管酸中毒（dRTA）可在BCN相关AKI的恢复阶段出现，可能是由于胆汁诱导损伤导致的肾小管功能障碍，这突出了肾恢复后密切进行代谢监测的必要性。BCN和dRTA的同时出现强调了对黄疸AKI患者进行连续电解质评估和酸碱评估的重要性，即使肾功能明显改善后也是如此。
Eur J Case Rep Intern Med. 2025-7-23
Arch Ital Urol Androl. 2025-6-30
Psychopharmacol Bull. 2024-7-8
1993
Clin Gastroenterol Hepatol. 2023-9
Cureus. 2022-3-29
Kidney Dis (Basel). 2017-12
Zotero 插件