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Distal renal tubular acidosis and acute tubulointerstitial nephritis: 3 case reports A case series described three men [exact ages at reactions onsets not stated], who developed distal renal tubular acidosis and acute tubulointerstitial nephritis during therapy with nivolumab or pembrolizumab. In addition, all three men also received omeprazole, which was believed to have contributed to the same [not all routes, dosages and outcomes stated; durations of treatments to reactions onsets not stated]. Case 1: A man in his early 60s presented to a clinic for evaluation of increased creatinine levels and electrolyte abnormalities, including metabolic acidosis and hypokalaemia. His medical history was notable for lung adenocarcinoma, for which he had been receiving pembrolizumab 200mg, alongside multiple other medications. A left lower lobe lobectomy was scheduled. Pembrolizumab was withheld. Prior to the surgery, there was no evidence of electrolyte abnormalities. However, during hospitalisation for lobe lobectomy, his creatinine levels varied between 1.1–1.2 mg/dL. During follow up after 6 weeks, prominent electrolyte level abnormalities were observed. He stated he had been taking omeprazole 40mg daily since a few weeks. Omeprazole was discontinued and replaced with ranitidine, and a nephrology consultation was scheduled. During nephrology consultation (3 months after the last dose of pembrolizumab), his creatinine level was elevated, and persistent nongap metabolic acidosis with hypokalaemia were noted. Urine microscopy was found to be bland, with a urinary protein-creatinine ratio of 0.4 g/g and urinary retinal-binding protein to creatinine ratio of 75 652 µg/g. He was diagnosed with distal renal tubular acidosis and was treated with sodium bicarbonate alongside potassium supplementation. Thereafter, he underwent ultrasound-guided kidney biopsy, which revealed chronic active tubulointerstitial nephritis with moderate arteriosclerosis. He received a prednisone taper. At the time of this report, pembrolizumab was not resumed. Case 2: A man in his 70s, who had been receiving IV nivolumab 240mg for 16 months for metastatic melanoma with BRAF mutation, presented for evaluation of electrolyte level abnormalities and elevated creatinine levels. He was also receiving omeprazole. One year later, while nivolumab was ongoing, he presented with fatigue, confusion and poor appetite. Subsequent analyses were notable for multiple electrolyte abnormalities and a creatinine level of 4.98 mg/dL, which had been was 1.27 mg/dL during the previous week, without evidence of electrolyte abnormalities. He was admitted and treated with sodium chloride [normal saline]. Acute tubulointerstitial nephritis was suspected due to the use of nivolumab and omeprazole. Therefore, both these drugs were discontinued. Follow-up tests revealed improved creatinine levels; however, metabolic acidosis worsened. He was treated with increased doses of prednisone and was referred to a nephrology clinic. A bland urine microscopy, with a urine protein/ osmolal