A 76-year-old man was referred to the hospital in September 2016, due to bilateral edema in his lower extremities and general fatigue. He had pancreaticoduodenectomy against pancreatic cancer in November, 2015, and had Tegafur, Gimeracil, Oteracil Potassium as postoperative chemotherapy which was discontinued because of the occurrence of pancytopenia. From April, 2016, nivolumab treatment at the dose of 0.5 mg/kg was started and continued until July, three times in total, which improved his symptoms for a certain period. However, from the beginning of September, 2016, he re-developed edema and fatigue. At visit, his serum creatinine (SCr) level increased from 0.8-0.9 mg/dL to 3.08 mg/dL, and he was hospitalized for further investigation. His past medical history was not remarkable, except for the history of treatment against lung tuberculosis in his 20's. Among his medication, rabeprazole 10 mg/day, Furosemide 10 mg/day, and spironolactone 25 mg/day were started recently. Other than that, he was taking levocarnitine 1500 mg/day and sennoside 24 mg/day. On physical examination, vital signs were unremarkable except for an increase of 5 kg in body weight in 4 months. His lungs were clear to auscultation, and bilateral pitting edema was noted in his lower extremities. His skin was dry, but no eruption nor rash were noted. Laboratory findings on admission are shown as Table 1. His SCr level was 3.08 mg/dL, and urinary protein or occult blood were both negative, although pyuria was evident without any eosinophil in urine cytology. Urinary excretion of beta2-miroglobulin and alpha1-microglubulin were high. A renal ultrasound showed hyperechoic parenchyma of bilateral kidneys without an evidence of hydronephrosis or enlargement of the both kidneys. Gallium scintigraphy showed increased gallium-67 uptake in both kidneys, which was compatible with the inflammation of AIN. A percutaneous renal biopsy was performed. Of 15 glomeruli, six were collapsed; however, no increase of mesangial matrix nor hypercellularity were represented. There was severe interstitial inflammation along with tubulitis in some parts. Among infiltrate lymphocytes, CD3+ T-lymphocytes were dominant, and infiltration over the basement membrane of CD8+ lymphocytes were seen. Some nuclei of tubular epithelial cells were variably sized, massively enlarged, irregularly shaped, and abnormally hyperchromatic occasionally. These morphological findings were indicative of those of karyomegalic changes. These epithelial cells were positive for Ki-67 in immunostaining, which suggested the regenerative changes in renal tubular epithelium. Interstitial fibrosis and tubular atrophy were observed in approximately 20% of the cortical area, according to the result of the Masson-trichrome staining. Overall, the changes represented drug-induced tubulointerstitial nephritis with karyomegalic epithelial changes. After the discontinuation of nivolumab treatment, his renal function had recovered gradually from 3.08 mg/dL to SCr level 1.84 mg/dL in 5 months. His renal function continued to partially improve, to which SCr level 1.42 mg/dL, approximately 1 year after the discontinuation of nivolumab treatment.