{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T22:27:53Z","timestamp":1787696873784,"version":"build-2784847793"},"reference-count":28,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01 DK090358"],"award-info":[{"award-number":["R01 DK090358"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2020,2]]},"abstract":"<jats:sec>\n                    <jats:title>Significance Statement<\/jats:title>\n                    <jats:p>The quality of a kidney obtained from a living donor is often inferred from the donor\u2019s age, risk factors, and kidney function. Little is known about the influence of a donated kidney\u2019s structural features on the risk of death-censored graft failure in the recipient. In an analysis of 2293 kidney donor-recipient pairs, the authors identified subclinical nephrosclerosis, larger nephron size (but not nephron number), and smaller medullary volume as structural predictors of death-censored graft failure that were independent of both donor and recipient clinical characteristics. These findings provide important insights into the factors that define the \u201cintrinsic quality\u201d of the living kidney donor graft at the time of donation, and support use of intraoperative biopsies to identify donor kidneys that are at higher risk for failure.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Nephrosclerosis, nephron size, and nephron number vary among kidneys transplanted from living donors. However, whether these structural features predict kidney transplant recipient outcomes is unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Our study used computed tomography (CT) and implantation biopsy to investigate donated kidney features as predictors of death-censored graft failure at three transplant centers participating in the Aging Kidney Anatomy study. We used global glomerulosclerosis, interstitial fibrosis\/tubular atrophy, artery luminal stenosis, and arteriolar hyalinosis to measure nephrosclerosis; mean glomerular volume, cortex volume per glomerulus, and mean cross-sectional tubular area to measure nephron size; and calculations from CT cortical volume and glomerular density on biopsy to assess nephron number. We also determined the death-censored risk of graft failure with each structural feature after adjusting for the predictive clinical characteristics of donor and recipient.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>The analysis involved 2293 donor-recipient pairs. Mean recipient follow-up was 6.3 years, during which 287 death-censored graft failures and 424 deaths occurred. Factors that predicted death-censored graft failure independent of both donor and recipient clinical characteristics included interstitial fibrosis\/tubular atrophy, larger cortical nephron size (but not nephron number), and smaller medullary volume. In a subset with 12 biopsy section slides, arteriolar hyalinosis also predicted death-censored graft failure.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Subclinical nephrosclerosis, larger cortical nephron size, and smaller medullary volume in healthy donors modestly predict death-censored graft failure in the recipient, independent of donor or recipient clinical characteristics. These findings provide insights into a graft\u2019s \u201cintrinsic quality\u201d at the time of donation, and further support the use of intraoperative biopsies to identify kidney grafts that are at higher risk for failure.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2019090964","type":"journal-article","created":{"date-parts":[[2020,1,23]],"date-time":"2020-01-23T16:15:15Z","timestamp":1579796115000},"page":"415-423","source":"Crossref","is-referenced-by-count":40,"title":["Kidney Structural Features from Living Donors Predict Graft Failure in the Recipient"],"prefix":"10.1681","volume":"31","author":[{"given":"Naim","family":"Issa","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension,"},{"name":"William J von Liebig Center for Transplantation and Clinical Regeneration,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Camden L.","family":"Lopez","sequence":"additional","affiliation":[{"name":"Division of Biomedical Statistics and Informatics, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aleksandar","family":"Denic","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandra J.","family":"Taler","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension,"},{"name":"William J von Liebig Center for Transplantation and Clinical Regeneration,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8372-0465","authenticated-orcid":false,"given":"Joseph J.","family":"Larson","sequence":"additional","affiliation":[{"name":"Division of Biomedical Statistics and Informatics, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Walter K.","family":"Kremers","sequence":"additional","affiliation":[{"name":"William J von Liebig Center for Transplantation and Clinical Regeneration,"},{"name":"Division of Biomedical Statistics and Informatics, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luisa","family":"Ricaurte","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Massini A.","family":"Merzkani","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariam Priya","family":"Alexander","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harini A.","family":"Chakkera","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Mayo Clinic Arizona, Scottsdale, Arizona; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark D.","family":"Stegall","sequence":"additional","affiliation":[{"name":"William J von Liebig Center for Transplantation and Clinical Regeneration,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua J.","family":"Augustine","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Cleveland Clinic, Cleveland, Ohio"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0338-7784","authenticated-orcid":false,"given":"Andrew D.","family":"Rule","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension,"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2020,1,23]]},"reference":[{"issue":"Suppl 1","key":"B1-20230829","doi-asserted-by":"crossref","first-page":"18","DOI":"10.1111\/ajt.14557","article-title":"OPTN\/SRTR 2016 annual data report: Kidney","volume":"18","author":"Hart","year":"2018","journal-title":"Am J 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