{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T21:46:49Z","timestamp":1777672009081,"version":"3.51.4"},"reference-count":44,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2019,5,12]],"date-time":"2019-05-12T00:00:00Z","timestamp":1557619200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["AN372\/16-2"],"award-info":[{"award-number":["AN372\/16-2"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["24-1"],"award-info":[{"award-number":["24-1"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Dysbiosis, bacterial translocation and systemic inflammation have been found to be associated with human and experimental forms of chronic kidney disease (CKD), but the functional contribution of the intestinal microbiota to CKD-related intestinal barrier dysfunction and CKD progression is unknown, especially in CKD secondary to hyperoxaluria and nephrocalcinosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>C57BL\/6N mice fed an oxalate-rich diet for either 10 or 20\u2009days developed reversible or progressive kidney disease, respectively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Oxalate-induced CKD manifested as azotaemia, renal anaemia and hyperkalaemia. CKD was associated with persistent dysbiosis and intestinal barrier dysfunction. Local as well as systemic inflammation was evident and partially persisted despite better renal function after returning to an oxalate-free diet, indicating some innate immune memory. Eradication of the microbiota with a combination of antibiotics improved intestinal barrier function but had no effect on renal function, nephrocalcinosis, kidney remodelling and atrophy compared with control mice not receiving antibiotics.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Together, in chronic oxalate nephropathy, the intestinal microbiota contributes to the CKD-related dysfunction of the intestinal barrier but not to the progression of nephrocalcinosis itself, as well to its related kidney atrophy and excretory dysfunction.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ndt\/gfz080","type":"journal-article","created":{"date-parts":[[2019,3,31]],"date-time":"2019-03-31T23:07:52Z","timestamp":1554073672000},"page":"86-97","source":"Crossref","is-referenced-by-count":6,"title":["The gut flora modulates intestinal barrier integrity but not progression of chronic kidney disease in hyperoxaluria-related nephrocalcinosis"],"prefix":"10.1093","volume":"35","author":[{"given":"Lukas","family":"Konrad","sequence":"first","affiliation":[{"name":"Nephrologisches Zentrum, Medizinische Klinik und Poliklinik IV, Klinikum der Universit\u00e4t, M\u00fcnchen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kirstin","family":"Andersen","sequence":"additional","affiliation":[{"name":"Nephrologisches Zentrum, Medizinische Klinik und Poliklinik IV, Klinikum der Universit\u00e4t, M\u00fcnchen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marie Sophie","family":"Kesper","sequence":"additional","affiliation":[{"name":"Nephrologisches Zentrum, Medizinische Klinik und Poliklinik IV, Klinikum der Universit\u00e4t, M\u00fcnchen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Santhosh V","family":"Kumar","sequence":"additional","affiliation":[{"name":"Nephrologisches Zentrum, Medizinische Klinik und Poliklinik IV, Klinikum der Universit\u00e4t, M\u00fcnchen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shrikant R","family":"Mulay","sequence":"additional","affiliation":[{"name":"Nephrologisches Zentrum, Medizinische Klinik und Poliklinik IV, Klinikum der Universit\u00e4t, M\u00fcnchen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hans-Joachim","family":"Anders","sequence":"additional","affiliation":[{"name":"Nephrologisches Zentrum, Medizinische Klinik und Poliklinik IV, Klinikum der Universit\u00e4t, M\u00fcnchen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2019,5,12]]},"reference":[{"key":"2025102312512130400_gfz080-B1","doi-asserted-by":"crossref","first-page":"1363","DOI":"10.1016\/j.ekir.2018.07.020","article-title":"Secondary oxalate nephropathy: a systematic review","volume":"3","author":"Lumlertgul","year":"2018","journal-title":"Kidney Int Rep"},{"key":"2025102312512130400_gfz080-B2","doi-asserted-by":"crossref","first-page":"649","DOI":"10.1056\/NEJMra1301564","article-title":"Primary hyperoxaluria","volume":"369","author":"Cochat","year":"2013","journal-title":"N Engl J Med"},{"key":"2025102312512130400_gfz080-B3","doi-asserted-by":"crossref","first-page":"656","DOI":"10.1016\/j.kint.2017.09.022","article-title":"The macrophage phenotype and inflammasome component NLRP3 contributes to nephrocalcinosis-related chronic kidney disease independent from IL-1-mediated tissue injury","volume":"93","author":"Anders","year":"2018","journal-title":"Kidney Int"},{"key":"2025102312512130400_gfz080-B4","first-page":"103","article-title":"Etiology of calcium oxalate nephrolithiasis in rats. 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