{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T05:21:44Z","timestamp":1790572904072,"version":"4.1.0"},"reference-count":32,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,4]]},"abstract":"<jats:sec>\n            <jats:title>Background.<\/jats:title>\n            <jats:p>Interstitial inflammation (i-INT) is the driver of T-cell\u2013mediated rejection. Its causes, pathophysiology, kinetics, and outcomes are poorly documented.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods.<\/jats:title>\n            <jats:p>The role of i-INT was evaluated in 2055 biopsies from 775 renal transplant recipients.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results.<\/jats:title>\n            <jats:p>i-INT was present in 374 (18.2% prevalence) from acute and subclinical rejection (67.4%); interstitial fibrosis and tubular atrophy (14.4%); BK virus nephropathy (BKVAN) 9.9%; and acute tubular necrosis (ATN with i-INT) in 5.9% of cases. i-INT was predicted by prior T-cell\u2013mediated rejection and BKVAN, human leukocyte antigen mismatch, cyclosporine therapy, and indication biopsy for dysfunction. It correlated with tubulitis, arteritis, and antibody markers within concurrent histology (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; 0.001). After treatment, renal functional recovery was best with histological ATN, milder i-INT, and early posttransplant biopsy times. The initial histological improvement of inflammation depended on baseline i-INT severity. Complete resolution to Banff i0 was predicted by early biopsy time, antilymphocyte therapy, recipient age, and medication compliance (all <jats:italic toggle=\"yes\">P<\/jats:italic> &lt; 0.001). Clearance i-INT was followed by delayed resolution of tubulitis (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; 0.001). i-INT was associated with histological ATN, renal dysfunction, and increased incident fibrosis on sequential pathology. Progressive fibrosis following related-rejection i-INT was dependent on tubulitis using multivariable analysis. In contrast, fibrogenesis after BKVAN or ATN was unrelated to inflammation. i-INT cases were followed by recurrent rejection in 35.3%, increased graft loss, and greater patient mortality. Multiple complementary outcome analyses determined the optimal lower diagnostic threshold for inflammation was Banff i1 score.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions.<\/jats:title>\n            <jats:p>i-INT is a heterogeneous pathological phenotype that results in adverse functional and structural outcomes, for which active and robust therapy should be considered.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1097\/tp.0000000000002887","type":"journal-article","created":{"date-parts":[[2019,8,1]],"date-time":"2019-08-01T16:18:39Z","timestamp":1564676319000},"page":"835-846","source":"Crossref","is-referenced-by-count":9,"title":["The Pathophysiology and Impact of Inflammation in Nonscarred Renal Interstitium: The Banff i Lesion"],"prefix":"10.1097","volume":"104","author":[{"given":"Brian J.","family":"Nankivell","sequence":"first","affiliation":[{"name":"Departments of Renal Medicine, Westmead Hospital, Tissue Pathology, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chow H.","family":"P\u2019Ng","sequence":"additional","affiliation":[{"name":"Diagnostic Oncology, ICPMR, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meena","family":"Shingde","sequence":"additional","affiliation":[{"name":"Diagnostic Oncology, ICPMR, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seethalakshmi","family":"Viswanathan","sequence":"additional","affiliation":[{"name":"Diagnostic Oncology, ICPMR, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anita","family":"Achan","sequence":"additional","affiliation":[{"name":"Diagnostic Oncology, ICPMR, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jasveen","family":"Renthawa","sequence":"additional","affiliation":[{"name":"Diagnostic Oncology, ICPMR, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raghwa N.","family":"Sharma","sequence":"additional","affiliation":[{"name":"Diagnostic Oncology, ICPMR, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeremy R.","family":"Chapman","sequence":"additional","affiliation":[{"name":"Departments of Renal Medicine, Westmead Hospital, Tissue Pathology, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"R1-20231002","doi-asserted-by":"crossref","first-page":"1596","DOI":"10.1681\/ASN.2017070800","article-title":"Four-dimensional imaging of T cells in kidney transplant rejection.","volume":"29","author":"Hughes","year":"2018","journal-title":"J Am Soc Nephrol"},{"key":"R2-20231002","doi-asserted-by":"crossref","first-page":"195","DOI":"10.3109\/01913128809058218","article-title":"Tubular ultrastructure in rejected human renal 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