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A new mouse model reveals that persistent asymptomatic hyperuricemia (approximately 15 mg\/dl) does not cause CKD, nor accelerate progression, unless UA crystallizes in acidic tubular fluid. Crystallization initially causes tubular injury, inflammation, and interstitial fibrosis, and subsequently granulomatous interstitial nephritis with perilesional proinflammatory M1-like macrophage infiltrates. Modulating the M1-like macrophage phenotype, but not JAK\/STAT inhibition, attenuates granulomatous nephritis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      The roles of asymptomatic hyperuricemia or uric acid (UA) crystals in CKD progression are unknown. Hypotheses to explain links between UA deposition and progression of CKD include that (\n                      <jats:italic toggle=\"yes\">1<\/jats:italic>\n                      ) asymptomatic hyperuricemia does not promote CKD progression unless UA crystallizes in the kidney; (\n                      <jats:italic toggle=\"yes\">2<\/jats:italic>\n                      ) UA crystal granulomas may form due to pre-existing CKD; and (\n                      <jats:italic toggle=\"yes\">3<\/jats:italic>\n                      ) proinflammatory granuloma-related M1-like macrophages may drive UA crystal-induced CKD progression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>MALDI-FTICR mass spectrometry, immunohistochemistry, 3D confocal microscopy, and flow cytometry were used to characterize a novel mouse model of hyperuricemia and chronic UA crystal nephropathy with granulomatous nephritis. Interventional studies probed the role of crystal-induced inflammation and macrophages in the pathology of progressive CKD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Asymptomatic hyperuricemia alone did not cause CKD or drive the progression of aristolochic acid I-induced CKD. Only hyperuricemia with UA crystalluria due to urinary acidification caused tubular obstruction, inflammation, and interstitial fibrosis. UA crystal granulomas surrounded by proinflammatory M1-like macrophages developed late in this process of chronic UA crystal nephropathy and contributed to the progression of pre-existing CKD. Suppressing M1-like macrophages with adenosine attenuated granulomatous nephritis and the progressive decline in GFR. In contrast, inhibiting the JAK\/STAT inflammatory pathway with tofacitinib was not renoprotective.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Asymptomatic hyperuricemia does not affect CKD progression unless UA crystallizes in the kidney. UA crystal granulomas develop late in chronic UA crystal nephropathy and contribute to CKD progression because UA crystals trigger M1-like macrophage-related interstitial inflammation and fibrosis. Targeting proinflammatory macrophages, but not JAK\/STAT signaling, can attenuate granulomatous interstitial nephritis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2020040523","type":"journal-article","created":{"date-parts":[[2020,9,16]],"date-time":"2020-09-16T20:18:17Z","timestamp":1600287497000},"page":"2773-2792","source":"Crossref","is-referenced-by-count":135,"title":["Only Hyperuricemia with Crystalluria, but not Asymptomatic Hyperuricemia, Drives Progression of Chronic Kidney Disease"],"prefix":"10.1681","volume":"31","author":[{"given":"Markus","family":"Sellmayr","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine IV, Ludwig-Maximilian's-University Hospital, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Moritz Roman","family":"Hernandez Petzsche","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine IV, Ludwig-Maximilian's-University Hospital, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiuyue","family":"Ma","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine IV, Ludwig-Maximilian's-University Hospital, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nils","family":"Kr\u00fcger","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine IV, Ludwig-Maximilian's-University Hospital, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helen","family":"Liapis","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri (retired) and Arkana Laboratories, Little Rock, Arkansas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6927-8252","authenticated-orcid":false,"given":"Andreas","family":"Brink","sequence":"additional","affiliation":[{"name":"Pharma Research and Early Development, Pharmaceutical Sciences, Roche Innovation Center Basel, F. 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