{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T19:42:32Z","timestamp":1790710952448,"version":"4.1.0"},"reference-count":35,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:00:00Z","timestamp":1787011200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Transplant."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Sodium-glucose cotransporter-2 inhibitors (SGLT2i) are established therapies in chronic kidney disease (CKD), but comparative data in kidney transplant recipients (KTR) remain limited.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We retrospectively matched 100 KTR receiving SGLT2i to 100 controls not receiving SGLT2i and assessed body mass index (BMI), HbA1c, urine albumin-to-creatinine ratio (uACR), estimated glomerular filtration rate (eGFR), serum potassium, RAAS inhibitor use, blood pressure, and safety outcomes at 6 and 12 months. Furthermore, we compared the Jaff\u00e9 and enzymatic methods to examine the effect of SGLT2i-associated glucosuria on urinary creatinine measurements and the resulting uACR.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      BMI decreased in the intervention group and increased in controls; the overall adjusted between-group difference across follow-up remained statistically significant. Descriptive between-group differences in HbA1c were observed at 6 and 12 months, but were not confirmed after multivariable adjustment. Neither uACR nor eGFR differed significantly at 12 months, despite an initial decline in eGFR at 6 months. Serum potassium remained stable over time. Hyperkalemia was associated with lower eGFR, but not with SGLT2i treatment, and RAAS inhibitor persistence did not differ between groups. No statistically detectable differences or clear new safety signals were observed for blood pressure, urinary tract infections, cardiovascular events, or hospitalizations during follow-up. Jaff\u00e9-based creatinine measurements were lower than enzymatic measurements, increasing calculated uACR by approximately 8.5% (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&amp;lt;\u20090.001), with rare albuminuria stage reclassification.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>SGLT2i use was associated with favorable metabolic changes, particularly a reduction in BMI, without evidence of increased potassium-related risk. No improvement in graft function or albuminuria was observed over 1 year. SGLT2i-associated glucosuria systematically increased Jaff\u00e9-based uACR estimates, although clinically relevant albuminuria reclassification was uncommon.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/frtra.2026.1927374","type":"journal-article","created":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T05:37:48Z","timestamp":1787031468000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["SGLT2 inhibitors in kidney transplant recipients: metabolic changes, potassium-related safety and implications for albuminuria assessment"],"prefix":"10.3389","volume":"5","author":[{"given":"Lino","family":"Henkel","sequence":"first","affiliation":[{"name":"Department of Medicine D, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa","family":"Ingmanns","sequence":"additional","affiliation":[{"name":"Department of Medicine D, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florian","family":"Westphal","sequence":"additional","affiliation":[{"name":"Department of Nephrology, University Hospital Zurich","place":["Zurich, Switzerland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Am\u00e9lie F.","family":"Menke","sequence":"additional","affiliation":[{"name":"Department of Medicine D, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hermann","family":"Pavenst\u00e4dt","sequence":"additional","affiliation":[{"name":"Department of Medicine D, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrich","family":"Jehn","sequence":"additional","affiliation":[{"name":"Nephrologisches Zentrum Emsland","place":["Lingen, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G\u00f6ran R.","family":"Boeckel","sequence":"additional","affiliation":[{"name":"Department of Medicine D, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Reuter","sequence":"additional","affiliation":[{"name":"Department of Medicine D, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,8,18]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"2123","DOI":"10.3390\/biomedicines13092123","article-title":"Nephroprotective mechanisms of SGLT2i: beyond the glucose-lowering effect","author":"Mazzieri","year":"2025","journal-title":"Biomedicines"},{"key":"B2","doi-asserted-by":"publisher","first-page":"1436","DOI":"10.1056\/NEJMoa2024816","article-title":"Dapagliflozin in 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