Abstract
Acute tubulointerstitial nephritis (ATIN) is an immunomediated cause of acute kidney injury. The prevalence of ATIN among the causes of acute kidney injury (AKI) is not negligible, especially those cases related to certain drugs. To date, there is a lack of reliable non-invasive diagnostic and follow-up markers. The gold standard for diagnosis is kidney biopsy, which shows a pattern of tubulointerstitial leukocyte infiltrate. The urinalysis findings can aid in the diagnosis but are no longer considered sensitive or specific. Atthe present time, there is a rising attentiveness tofinding trustworthy biomarkers of the disease, with special focus in urinary cytokines and chemokines that may reflect kidney local inflammation. Cell-based tests are of notable interest to identify the exact drug involved in hypersensitivity reactions to drugs, manifesting as ATIN. Certain single-nucleotide polymorphisms in HLA or cytokine genes may confer susceptibility to the disease according to pathophysiological basis. In this review, we aim to critically examine and summarize the available evidence on this topic.
Highlights
Acute tubulointerstitial nephritis (ATIN) is an immunomediated disease affecting the tubulointerstitial area of the kidneys
A myriad of etiologies can lead to ATIN, drug-induced ATIN is the most common, accounting for 3–14% of biopsy-proven acute kidney injury (AKI) [2] and 70–90% of ATIN cases [3]
Red blood cell (RBC) casts were once thought to be specific for glomerular disease, up to one third of ATIN patients exhibit RBC, probably
Summary
Acute tubulointerstitial nephritis (ATIN) is an immunomediated disease affecting the tubulointerstitial area of the kidneys. TECs present antigens to dendritic cells, which in turn migrate to regional lymph nodes, activate specific T cells, and integrate innate and adaptive immune responses [5]. Those activated T cells infiltrate the renal parenchyma and amplify inflammation through increased secretion of cytokines and the recruitment of other inflammatory cells [4]. It has been hypothesized that drugs can directly damage TECs and induce necroptosis This is a recently-described form of cell death, halfway between necrosis and apoptosis, leading to the release of proinflammatory cytokines and the recruitment of innate immune system cells. Based on the predominance of an inflammatory component in the kidneys of ATIN, some classical and novel biomarkers, reviewed hereunder, may serve in the diagnosis, prognosis, and follow-up of this disease
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