Refining of zirconium by tributyl phosphate in pulsed packed columns

El-Yamani, I. S.; El-Aleim, F. A. Abd

doi:10.1016/0304-386x(84)90028-8

Cited by 2 publications

(1 citation statement)

References 5 publications

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“…Existing studies have demonstrated that the mechanism of ICIs-related renal injury supports the "multiple hit" or "brake release" theory, affecting the immune tolerance of T cells to renal intrinsic antigen (autoimmune-related) or concomitant drugs (drug-induced) in the presence of PD 1, PD L1, and CTLA 4 inhibitors, activated T cells in ltrate in the renal parenchyma, and release cytokines leading to renal injury [1] . Its main clinical manifestation is AKI; the most common pathological type is tubulointerstitial nephritis (TIN) [2] , and other pathological changes include thrombotic microangiopathy [3] , immune complex glomerulonephritis [4] , anti-GBM glomerulonephritis [5] , glomerular minimal change disease, membranous nephropathy, immune glomerulonephritis, and IgA nephropathy [6] . If the patient has elevated serum creatinine after receiving ICIs (the patient's serum creatinine level is 1.5 times higher than before ICI treatment [7] ), the possibility of ICI-related AKI should be considered in clinical diagnosis and treatment.…”

Section: Discussionmentioning

confidence: 99%

A Case Report of Multiple Systemic Immune Adverse Reaction Caused by Immune Checkpoint Inhibitors in Lung Cancer

Wang,

Li,

Dong

2023

Preprint

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Background: Immune checkpoint inhibitors(ICIs) have been shown to have antitumor activity in various solid tumors. With the increase in clinical applications of ICIs, reports of immune-related adverse events (irAEs) have also increased. ICI-associated renal adverse effects are rare, accompanying Multiple Systemic Immune Adverse Reaction. This article reports a case of a lung cancer patient who developed multisystemic adverse effects after PD-1 inhibitor application: acute kidney injury, rash, thyroiditis, and pneumonia. Renal biopsy histopathological results acute tubulointerstitial nephritis. His multisystemic dysfunction recovered within 3 months of treatment with prednisolone in addition to discontinuation of tislelizumab. Glucocorticoids are the main treatment, and close attention should be paid to the presence or absence of new irAEs during the process. Besides,Despite the patient’s eventual discontinuation of antitumor therapy due to severe irAEs, a significant and durable therapeutic response was observed

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