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Cited by 650

The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.

Clinicopathological features of acute kidney injury associated with immune checkpoint inhibitors

Open access
Cortazar, Frank B., Marrone, Kristen A., Troxell, Megan L., Ralto, Kenneth M., Hoenig, Melanie P., Brahmer, Julie R., Le, Dung T., Lipson, Evan J., Glezerman, Ilya G., Wolchok, Jedd, Cornell, Lynn D., Feldman, Paul, Stokes, Michael B., Zapata, Sarah A., Hodi, F. Stephen, Ott, Patrick A., Yamashita, Michifumi, Leaf, David E.·2016·Kidney International
DOI 10.1016/j.kint.2016.04.008
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Abstract

Immune checkpoint inhibitors (CPIs), monoclonal antibodies that target inhibitory receptors expressed on T cells, represent an emerging class of immunotherapy used in treating solid organ and hematologic malignancies. We describe the clinical and histologic features of 13 patients with CPI-induced acute kidney injury (AKI) who underwent kidney biopsy. Median time from initiation of a CPI to AKI was 91 (range, 21 to 245) days. Pyuria was present in 8 patients, and the median urine protein to creatinine ratio was 0.48 (range, 0.12 to 0.98) g/g. An extra-renal immune-related adverse event occurred prior to the onset of AKI in 7 patients. Median peak serum creatinine was 4.5 (interquartile range, 3.6-7.3) mg/dl with 4 patients requiring hemodialysis. The prevalent pathologic lesion was acute tubulointerstitial nephritis in 12 patients, with 3 having granulomatous features, and one thrombotic microangiopathy. Among the 12 patients with acute tubulointerstitial nephritis, 10 received treatment with glucocorticoids, resulting in complete or partial improvement in renal function in 2 and 7 patients, respectively. However, the two patients with acute tubulointerstitial nephritis not given glucocorticoids had no improvement in renal function. Thus, CPI-induced AKI is a new entity that presents with clinical and histologic features similar to other causes of drug-induced acute tubulointerstitial nephritis, though with a longer latency period. Glucocorticoids appear to be a potentially effective treatment strategy. Hence, AKI due to CPIs may be caused by a unique mechanism of action linked to reprogramming of the immune system, leading to loss of tolerance.

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Metadata

Authors
Cortazar, F. B., Marrone, K. A., Troxell, M. L., Ralto, K. M., Hoenig, M. P., Brahmer, J. R., Le, D. T., Lipson, E. J., Glezerman, I. G., Wolchok, J., Cornell, L. D., Feldman, P., Stokes, M. B., Zapata, S. A., Hodi, F. S., Ott, P. A., Yamashita, M., & Leaf, D. E.
Venue
Kidney International
Publisher
Elsevier BV
Published
2016-09
Volume
90
Issue
3
Pages
638-647
ISSN
0085-2538 (ISSN-L)
DOI
10.1016/j.kint.2016.04.008
OpenAlex
W2413514895
Cited by
650
References
10
FWCI
25.50
Type
journal article
Language
en
Open access
bronze

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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