Key Clinical MessageIn the treatment of immunotherapy with immune checkpoint inhibitors, we often experience immune‐related adverse event which manifest most frequently as a skin disorder, and very rarely as a renal disorder. In our manuscript, we report the case of a 71‐year‐old man with nivolumab‐induced severe acute kidney injury (AKI) in which the time from treatment initiation to the onset of AKI was the longest among the previously reported cases (377 days). Prolonged follow‐up is therefore warranted to detect late‐onset AKI.

A 60-year-old man presented to the emergency department with lightheadedness. He had severe hyponatremia (109 mEq/L) complicated by acute kidney injury (AKI) (serum creatinine: 9.08 mg/dL). Because he was somnolescent, his hyponatremia was initially treated by administering a 130-mL bolus of 3% saline 2 to 5 times per day for 5 days. He subsequently underwent intermittent hemodialysis without any neurological problems. Previous reports have described patients with hyponatremia and AKI being treated with continuous renal replacement therapy. However, our strategy might be a feasible, low-cost treatment strategy of treating patients with hyponatremia and AKI who do not require immediate hemodialysis.

ObjectiveAutosomal recessive spinocerebellar ataxia type 9 (SCAR9) has received attention due to its potential response to coenzyme Q10 (CoQ10) supplementation; however, the response has so far been limited and variable.MethodsWe report a SCAR9 patient with severe hypophosphatemia who responded well to CoQ10 and phosphate repletion.ResultsA 70-year-old man (the offspring of a consanguineous marriage) presented with cerebellar ataxia and intense fatigue after exercise. Whole-exome sequencing identified a novel homozygous deletion mutation (NM_020247.5:c.1218_1219del) inCOQ8A. We thus diagnosed him with SCAR9. Supplementation of CoQ10 alleviated his symptoms, with the Scale for the Assessment and Rating of Ataxia (SARA) dropping from 16 to 14. During the course of the disease, he demonstrated continuous hypophosphatemia caused by renal phosphate wasting. Gait dysfunction due to weakness and eye movement was partially alleviated, and SARA dropped from 17 to 13 after phosphate repletion.DiscussionPhosphate repletion should be considered for patients with severe hypophosphatemia without any apparent subjective symptoms. In this case, phosphate repletion could have improved myopathy leading to partial improvement in the patient's symptoms. Further analyses regarding the association between COQ8A mutation and phosphate wasting are required to elucidate the detailed pathogenesis.Classification of EvidenceThis provides Class IV evidence. This is a single observational study without controls.

A 68-year-old male with gastric cancer was treated with tegafur/gimeracil/oteracil and oxaliplatin for 6 months. Thereafter, he was treated with paclitaxel and ramucirumab for 3 months. However, neither regimen had much effect. Thus, he was treated with nivolumab for 2 months, but he developed proteinuria, microhematuria, and an acute kidney injury. A kidney biopsy revealed occasional swollen endothelial cells and proliferating mesangial cells. Few abnormal findings were seen in the tubules or interstitial tissue. Immunofluorescent staining showed segmental immunoglobulin A and complement component 3 deposition, in the mesangial area. Electron microscopy showed a small amount of electron-dense deposits in the paramesangial area and swollen endothelial cells. Mesangial interposition, the loss of endothelial cell fenestration, and subendothelial edema were also observed. Furthermore, foot process effacement and villous transformation of epithelial cells were noted. After the discontinuation of nivolumab, the patient's renal function gradually improved, and his proteinuria disappeared. Nivolumab treatment was restarted at that time because of cancer progression; however, it was ineffective. No occult blood was detected from 7 months after the administration of the last dose of nivolumab. This is a unique case, in which a kidney biopsy revealed evidence of nivolumab-associated glomerular endothelial injury.