Recently, there have been reports of new cases of acute kidney injury (AKI) after coronavirus disease 2019 (COVID-19) vaccination. Podocytic damage, IgA nephropathy, vasculitis, tubulointerstitial damage, and thrombotic microangiopathy have been reported as the causes. However, there are no reports of acute tubular injury (ATI) as the sole cause of AKI. In this case, a 54-year-old man with type 2 diabetes visited a local physician. He was highly obese with a body mass index of 36 kg/m2. He was treated with metformin and insulin. Diabetic retinopathy, urinary protein, and occult blood were absent. He had received four COVID-19 vaccines; three were from Pfizer and one from Moderna. He was referred to our hospital 5 days after receiving the fourth dose of the Pfizer-BioNTech COVID-19 vaccine. He had stage 3 AKI. Urinary findings revealed the presence of new proteinuria and glomerular occult blood. Steroids were introduced on the day of admission for rapidly progressive glomerulonephritis. A renal biopsy was performed on the second day, with results obtained on the fifth day revealing no findings other than ATI. The patient was therefore deemed unamenable to steroids. After steroid discontinuation, renal function recovered spontaneously, and urinalysis abnormalities disappeared. In this case, ATI was the sole pathogenesis of COVID-19 vaccine-induced AKI, and treatment with immunosuppressive drugs was not necessary.

Coronavirus disease 2019 (COVID-19) is a severe respiratory infection that can be fatal in unvaccinated individuals; however, acute kidney injury (AKI) is a rare adverse reaction to COVID-19 vaccination. AKI resulting from multiple conditions can have severe consequences, including end-stage renal failure, if not treated with immunosuppressive agents. However, acute tubular injury (ATI) as the sole cause of AKI has not been previously reported. Herein, we discuss an obese 54-year-old man with type 2 diabetes who received four COVID-19 vaccines; three from Pfizer and one from Moderna. Diabetic retinopathy, urinary protein, and occult blood were absent with no other underlying diseases. There was no history of COVID-19 infection. He was referred to our hospital 5 days after receiving the fourth Pfizer-BioNTech COVID-19 vaccine dose with stage 3 AKI. Urinary findings revealed new proteinuria and glomerular occult blood. Physical examination and infection testing were unremarkable. Steroids were introduced on admission for rapidly progressive glomerulonephritis. A renal biopsy performed on Day 2 revealed only ATI. Therefore, steroids were discontinued on Day 5, after which renal function recovered spontaneously, and urinalysis abnormalities disappeared. Renal function remained normal during follow-up. We report a case of AKI with severe renal dysfunction after COVID-19 vaccination, wherein renal biopsy effectively determined the disease status (ATI), which did not require immunosuppressive treatment.

Background Oxaliplatin is an anticancer therapy for pancreatic, gastric, and colorectal cancers. It is also used in patients with carcinomas of unknown primary sites. Oxaliplatin is associated with less frequent renal dysfunction than other conventional platinum-based drugs such as cisplatin. Albeit, there have been several reports of acute kidney injury with frequent use. In all cases, renal dysfunction was temporary and did not require maintenance dialysis. There have been no previous reports of irreversible renal dysfunction after a single dose of oxaliplatin. Case presentation Previous reports of oxaliplatin-induced renal injury occurred after patients received multiples doses. In this study, a 75-year-old male with unknown primary cancer and underlying chronic kidney disease developed acute renal failure after receiving the first dose of oxaliplatin. Suspected of having drug-induced renal failure through an immunological mechanism, the patient was treated with steroids; however, treatment was ineffective. Renal biopsy ruled out interstitial nephritis and revealed acute tubular necrosis. Renal failure was irreversible, and the patient subsequently required maintenance hemodialysis. Conclusions We provide the first report of pathology-confirmed acute tubular necrosis after the first dose of oxaliplatin which led to irreversible renal dysfunction and maintenance dialysis.

Background Vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic (VEXAS) syndrome is caused by mutations in the ubiquitin-activating enzyme 1 (UBA1) gene and is characterised by the overlap of multiple autoinflammatory and haematologic disorders. It is a rare disease first described in December 2020. Case presentation: We report the case of a 67-year-old Japanese man undergoing peritoneal dialysis (PD) for recurrent aseptic peritonitis caused by VEXAS syndrome. He presented with an unexplained fever, headache, abdominal pain, conjunctival hyperaemia, ocular pain, auricular pain, arthralgia, and inflammatory skin lesions. Laboratory investigations showed a high serum C-reactive protein concentration and an increased white blood cell count in the PD effluent. He was treated with antibiotics for PD-related peritonitis but to no avail. Fluorine-18-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography demonstrated intense FDG uptake in the left superficial temporal artery, nasal septum, and bilateral auricles. The working diagnosis was giant cell arteritis, and the patient was treated with oral prednisolone (PSL) 15 mg daily, with a good response. However, the PSL dose could not be tapered to less than 10 mg daily because of auricular pain, skin lesions, and PD effluent turbidity. Tocilizumab was administered every two weeks as a steroid-sparing agent; hence, the PSL dose could be tapered to 2 mg daily without any symptoms. Sanger sequencing of his peripheral blood sample revealed a mutation affecting methionine-41 (c.122 T > C; p.Met41Thr) of the UBA1 gene. We made the final diagnosis of VEXAS syndrome. He had a flare of VEXAS syndrome at a PSL of 1 mg daily with cloudy PD effluent, conjunctival hyperaemia, arthralgia, auricular chondritis, and inflammatory skin lesions, such as Sweet's syndrome, on his upper limbs and neck. Increasing the PSL dose to 11 mg daily relieved the symptoms within a few days. Conclusions VEXAS syndrome causes turbid PD effluent without infection. When peritonitis is observed in patients on PD, nephrologists and general physicians should consider the possibility of aseptic peritonitis due to autoimmune diseases, including VEXAS syndrome, and pay attention to their systemic findings.