Abstract
Introduction: Immune checkpoint inhibitors (CPIs) represent novel new cancer immunotherapy agents. The use of nivolumab has been linked with immune mediated acute interstitial nephritis (AIN). Case Presentation: We present the case of a patients with recurrent hepatocellular carcinoma who developed severe Fanconi syndrome, as evidenced by hyperchloremic metabolic acidosis, hypokalemia, hypophosphatemia, glucosuria, aminoaciduria, 8 months after initiating treatment with nivolumab, without any evidence of acute renal insufficiency. Conclusion: Clinicians need to be aware of the renal side effects of new novel cancer immunotherapy agents, such as, immune CPIs
Highlights
Immune checkpoint inhibitors (CPIs) represent novel new cancer immunotherapy agents
Case Presentation: We present the case of a patients with recurrent hepatocellular carcinoma who developed severe Fanconi syndrome, as evidenced by hyperchloremic metabolic acidosis, hypokalemia, hypophosphatemia, glucosuria, aminoaciduria, 8 months after initiating treatment with nivolumab, without any evidence of acute renal insufficiency
Implication for health policy/practice/research/medical education: Clinicians need to be aware of the renal side effects of new novel cancer immunotherapy agents, such as, immune checkpoint inhibitors
Summary
Immune checkpoint inhibitors (CPIs) represent novel cancer immunotherapy agents. They are used in treating hematological and solid organ malignancies. The immune CPI monoclonal antibodies either block the interaction between PD-1 on activated T lymphocytes and PD-L1 on tumor cell surface that results in anti-proliferation and tumor apoptosis, or block the interaction of CTLA-4 on T lymphocytes and B7 (CD80/86) on antigen presenting cells that leads to augmented costimulatory pathway activation of effector T lymphocytes Both scenarios lead to enhanced immune reactivity and may lead to autoimmunity [1]. The patient has declined follow up in the renal clinic This patient’s presentation was consistent with acquired Fanconi syndrome (non-anion gap hyperchloremic metabolic acidosis due to proximal renal tubular acidosis (pRTA), hypokalemia, hypophosphatemia, aminoaciduria, and glucosuria) due to the CPI nivolumab. He did not have other conditions that would explain the above findings such as paraproteinemia. He had no prior history of electrolyte problems based on review of prior laboratory studies
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