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While murine models of CaOx stone disease are established, many lack translational features for therapeutic evaluation, including in vivo assessment of kidney function and molecular profiling of renal inflammation. We refined the glyoxylate\u2011induced CaOx mouse model by incorporating non\u2011invasive transdermal glomerular filtration rate (\n                    <jats:italic>t<\/jats:italic>\n                    GFR) measurements to enable longitudinal assessment of kidney function. This platform was used to investigate the renoprotective role of the anti\u2011inflammatory cytokine interleukin\u201137 (IL\u201137). Because mice do not express IL\u201137, we used IL\u201137 transgenic (IL\u201137tg) mice that express the human\n                    <jats:italic>IL37b<\/jats:italic>\n                    isoform. Male wild\u2011type and IL\u201137tg mice received daily intraperitoneal glyoxylate to induce CaOx deposition. Crystal burden and tubular injury were quantified using digital image analysis of whole\u2011kidney sections. Kidney function was assessed using\n                    <jats:italic>t<\/jats:italic>\n                    GFR and validated by serum creatinine, blood urea nitrogen (BUN), and symmetric dimethylarginine (SDMA). Renal inflammation was profiled using an RT\u00b2 Profiler PCR Array, with key transcripts validated by qPCR. CaOx deposition peaked on day 6, coinciding with tubular injury and impaired kidney function in both wild\u2011type and IL\u201137tg mice, as evidenced by reduced\n                    <jats:italic>t<\/jats:italic>\n                    GFR and elevated BUN, creatinine, and SDMA. Stone formation triggered a robust inflammatory response, with 46 of 84 genes upregulated\u2009&gt;\u20093\u2011fold in wild\u2011type mice. IL\u201137 expression did not alter crystal burden, kidney injury, kidney function, or inflammatory gene expression. These findings establish a refined murine CaOx model incorporating kidney function and molecular endpoints and demonstrate that IL\u201137 does not confer renal protection in glyoxylate\u2011induced stone disease.\n                  <\/jats:p>","DOI":"10.1007\/s00240-026-02061-7","type":"journal-article","created":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T21:47:02Z","timestamp":1791668822000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Interleukin-37 does not confer protection against stone formation or kidney injury at the peak of disease in a murine calcium oxalate model"],"prefix":"10.1007","volume":"54","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-9995-6702","authenticated-orcid":false,"given":"Nirmal P.","family":"Bhatt","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Theresa T. 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