BACKGROUND: Acute renal impairment is a relatively rare complication of anti-tumour immunotherapy. The incidence of renal toxicity due to immuno-oncological therapy is relatively low, approximately 2% in patients treated with PD-1/PD-L1 inhibitors and 4.5% with combination treatments with PD-1/PD-L1 therapy and a CTLA-4 inhibitor. The most common underlying pathology is acute tubulointerstitial nephritis. Autoimmune nephropathy presenting as a electrolyte imbalance may also occur during immuno-oncological therapy. Discontinuation of immunotherapy and corticosteroid therapy are indicated in patients with moderate to severe renal toxicity. CASE: A 61-year-old patient with metastatic renal cell carcinoma was admitted to hospital after 7 months of treatment with nivolumab for general deterioration, severe weakness, nausea, and anorexia. Laboratory examinations showed worsening of the glomerular filtration rate, severe hyperkalaemia, and metabolic acidosis. Thyroid hormone and cortisol levels were within normal ranges. Renal tubular acidosis resulting from immuno-oncological therapy was diagnosed, and treatment with methylprednisolone was initiated. Electrolyte abnormalities and symptoms improved rapidly, after which the dose of prednisone was gradually reduced; however, after a reduction to 5 mg daily, hyperkalaemia recurred and the patient was kept on a maintenance dose of 10 mg prednisone administered orally on a daily basis thereafter. Immunotherapy was not reintroduced. CONCLUSION: Renal toxicity following immuno-oncological therapy usually presents initially as an increase in the serum creatinine level without any clinical signs or symptoms. Electrolyte disturbances, oliguria, anuria, and swelling may develop gradually. Endocrine and metabolic disorders such as new-onset type 1 diabetes mellitus, hypophysitis, adrenal insufficiency, and hypothyroidism should be excluded as possible causes of electrolyte abnormalities. Corticosteroids at the usual immunosuppressive dose are the treatment of choice. The prognosis is generally favourable because renal toxicity responds well to corticosteroid treatment regardless of the underlying pathology.

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