Abstract
Acute kidney injury in patients who suffer a malignancy is a common complication. Due to its high prevalence and effective treatment, one of the most frequent causes that both oncologists and nephrologists must be aware of is acute tubulointerstitial nephritis (ATIN). ATIN is an immunomediated condition and the hallmark of the disease, with the presence of a tubulointerstitial inflammatory infiltrate in the renal parenchyma. This infiltrate is composed mainly of T lymphocytes that can be accompanied by macrophages, neutrophils, or eosinophils among other cells. One of the major causes is drug-related ATIN, and some antineoplastic treatments have been related to this condition. Worthy of note are the novel immunotherapy treatments aimed at enhancing natural immunity in order to defeat cancer cells. In the context of the immunosuppression status affecting ATIN patients, some pathogen antigens can trigger the development of the disease. Finally, hematological malignancies can also manifest in the kidney leading to ATIN, even at the debut of the disease. In this review, we aim to comprehensively examine differential diagnosis of ATIN in the setting of a neoplastic patient.
Highlights
Acute tubulointerstitial nephritis (ATIN) is a frequent cause of acute kidney injury (AKI)
We aim to summarize the different causes of ATIN in the oncological population with the focus on its pathophysiology
Immune checkpoint inhibitors (ICI) are monoclonal antibodies directed against programmed cell death-1 (PD-1), PD-1 ligand 1 (PD-L1), and cytotoxic T lymphocyte antigen
Summary
Laura Martínez-Valenzuela 1,2 , Juliana Draibe 1,2, *, Xavier Fulladosa 1,2,3 , Montserrat Gomà 4 , Francisco Gómez 1 , Paula Antón 1 , Josep María Cruzado 1,2,3 and Joan Torras 1,2,3, *. Clinical Science Department, Campus de Bellvitge, Barcelona University, L’Hospitalet de Llobregat, 08907 Barcelona, Spain
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