Evidence map›Paper›PMID 40786557›Full record

ArticleEuropean journal of case reports in internal medicine2025

Distal Renal Tubular Acidosis Secondary to Hyperbilirubinemia.

Fawzi Srour, Aline Pourcelet, Ishak Beklevic, Guillaume Benoit, Serge Treille de Grandsaigne, Nathan Neveux

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Article in European journal of case reports in internal medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Fawzi SrourDepartment of Internal Medicine, Medical School ULB, Brussels, Belgium.
Aline PourceletDepartment of Nephrology, University Hospital Marie-Curie, Charleroi, Belgium.
Ishak BeklevicDepartment of Nephrology, University Hospital Marie-Curie, Charleroi, Belgium.
Guillaume BenoitDepartment of Nephrology, University Hospital Marie-Curie, Charleroi, Belgium.
Serge Treille de GrandsaigneDepartment of Nephrology, University Hospital Marie-Curie, Charleroi, Belgium.
Nathan NeveuxDepartment of Nephrology, University Hospital Marie-Curie, Charleroi, Belgium.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

acute kidney injuryBile cast nephropathydistal renal tubular acidosiselectrolyte imbalancehyperbilirubinemia

Identifiers

PMID40786557
PMCPMC12331275

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