Distal Renal Tubular Acidosis Secondary to Hyperbilirubinemia

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.

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).

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.

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.

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.