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Abstract: FR-PO282

Hyperacute Immune Checkpoint Inhibitor-Associated Acute Tubulointerstitial Nephritis (ICI-ATIN) Followed by ICI-Renal Tubular Acidosis (RTA): A Case Report

Session Information

Category: Onconephrology

  • 1700 Onconephrology


  • Tan, Hui Zhuan, Singapore General Hospital, Singapore, Singapore
  • Kanesvaran, Ravindran, National Cancer Center Singapore, Singapore, Singapore
  • Law, Yi Chye, National Cancer Center Singapore, Singapore, Singapore
  • Lee, Joycelyn Jie Xin, National Cancer Center Singapore, Singapore, Singapore

Hyperacute renal immune-related adverse events (irAEs) are rare. Immune-checkpoint inhibitor related renal tubular acidosis (ICI-RTA) has been described, but its true incidence is unknown. We report a case of biopsy proven hyperacute ICI-related acute tubulo-interstitial nephritis (ICI-ATIN) with probable ICI-RTA developing after completion of steroid therapy.

Case Description

A 67-year-old Skih male was referred for non-oliguric KDIGO 3 AKI (sCr 219μmol/L; baseline sCr 62μmol/L) and fever occurring 9 days after his first cycle of ipilimumab and nivolumab for treatment of metastatic clear cell renal cell carcinoma. Investigations showed pyuria (urinary leukocytes 168/μL) and subnephrotic range proteinuria (uPCR 2.42g/g). C-reactive protein was raised at 205mg/L. Renal obstruction was excluded. There was no exposure to nephrotoxic drugs.

Empirical broad-spectrum antibiotics was commenced. Progression of AKI (peak sCr 351μmol/L) prompted the initiation of prednisolone (60mg/day) for treatment of presumptive ICI-ATIN, once infection screen returned negative. ATIN was subsequently confirmed on kidney biopsy. Favourable response was observed, and prednisolone was tapered over 6 weeks. ICI was not resumed. Tyrosine kinase inhibitor was commenced.

Gradually worsening hypokalemia, normal-gap metabolic acidosis, hypophosphatemia were observed shortly after completion of steroid therapy. RTA was clinically suspected. However, concurrent pulmonary infection contraindicated further steroid therapy. Electrolyte/alkali replacement was commenced. Gradual dose de-escalation, but not cessation, of replacement was successful during 8 months of follow-up.


ICI-ATIN should be suspected in all patients on ICI with AKI, regardless of timing of presentation. Differentials of AKI with fever in this context include sepsis-associated AKI, cytokine release syndrome and ICI-ATIN. Diagnosis may be challenging without kidney biopsy. An early, empiric trial of steroids may be considered as soon as infection is excluded. Limited evidence suggests that patients with hyperacute irAE(s) may develop further toxicities despite steroid therapy and cessation of ICI. ICI-RTA was a probable differential in our case. Steroid therapy remains the mainstay of treatment of ICI-RTA. It is uncertain if ICI-RTA can be transient or will persist as a chronic toxicity in patients managed without steroids.