{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T07:11:35Z","timestamp":1789456295481,"version":"build-2803163510"},"reference-count":39,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2024,1,27]],"date-time":"2024-01-27T00:00:00Z","timestamp":1706313600000},"content-version":"vor","delay-in-days":1152,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2022,7,8]],"date-time":"2022-07-08T00:00:00Z","timestamp":1657238400000},"content-version":"vor","delay-in-days":584,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["asbmr.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2020,12,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) represents an FGF23-independent disease caused by biallelic variants in the solute carrier family 34-member 3 (SLC34A3) gene. HHRH is characterized by chronic hypophosphatemia and an increased risk for nephrocalcinosis and rickets\/osteomalacia, muscular weakness, and secondary limb deformity. Biochemical changes, but no relevant skeletal changes, have been reported for heterozygous SLC34A3 carriers. Therefore, we assessed the characteristics of individuals with biallelic and monoallelic SLC34A3 variants. In 8 index patients and 5 family members, genetic analysis was performed using a custom gene panel. The skeletal assessment comprised biochemical parameters, areal bone mineral density (aBMD), and bone microarchitecture. Pathogenic SLC34A3 variants were revealed in 7 of 13 individuals (2 homozygous, 5 heterozygous), whereas 3 of 13 carried monoallelic variants of unknown significance. Whereas both homozygous individuals had nephrocalcinosis, only one displayed a skeletal phenotype consistent with HHRH. Reduced to low-normal phosphate levels, decreased tubular reabsorption of phosphate (TRP), and high-normal to elevated values of 1,25-OH2-D3 accompanied by normal cFGF23 levels were revealed independently of mutational status. Interestingly, individuals with nephrocalcinosis showed significantly increased calcium excretion and 1,25-OH2-D3 levels but normal phosphate reabsorption. Furthermore, aBMD Z-score &amp;lt;\u22122.0 was revealed in 4 of 8 heterozygous carriers, and HR-pQCT analysis showed a moderate decrease in structural parameters. Our findings highlight the clinical relevance also of monoallelic SLC34A3 variants, including their potential skeletal impairment. Calcium excretion and 1,25-OH2-D3 levels, but not TRP, were associated with nephrocalcinosis. Future studies should investigate the effects of distinct SLC34A3 variants and optimize treatment and monitoring regimens to prevent nephrocalcinosis and skeletal deterioration. \u00a9 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).<\/jats:p>\n                  <jats:p>Abstract<\/jats:p>\n                  <jats:p>Half and 5 of 8 heterozygous SLC34A3 carriers had osteoporosis and a history of fractures, respectively. Individuals with detected nephrocalcinosis had significantly increased 1,25-OH2-D3 levels and urinary calcium excretion but normal phosphate reabsorption rates. Therefore, optimized treatment and monitoring regimens are required to prevent nephrocalcinosis and skeletal deterioration.<\/jats:p>","DOI":"10.1002\/jbmr.4630","type":"journal-article","created":{"date-parts":[[2022,6,11]],"date-time":"2022-06-11T04:09:53Z","timestamp":1654920593000},"page":"1580-1591","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Clinical Spectrum of Hereditary Hypophosphatemic Rickets With Hypercalciuria (HHRH)"],"prefix":"10.1093","volume":"37","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5218-8442","authenticated-orcid":false,"given":"Julian","family":"St\u00fcrznickel","sequence":"first","affiliation":[{"name":"Department of Trauma and Orthopaedic Surgery University Medical Center Hamburg-Eppendorf Hamburg Germany"},{"name":"Department of Osteology and Biomechanics University Medical Center Hamburg-Eppendorf Hamburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fiona","family":"Heider","sequence":"additional","affiliation":[{"name":"Department of Osteology and Biomechanics University Medical Center Hamburg-Eppendorf Hamburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alena","family":"Delsmann","sequence":"additional","affiliation":[{"name":"Department of Osteology and Biomechanics University Medical Center Hamburg-Eppendorf Hamburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"G\u00f6del","sequence":"additional","affiliation":[{"name":"III. 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Department of Medicine University Medical Center Hamburg-Eppendorf Hamburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4582-9838","authenticated-orcid":false,"given":"Uwe","family":"Kornak","sequence":"additional","affiliation":[{"name":"Institute of Human Genetics University Medical Center G\u00f6ttingen G\u00f6ttingen Germany"},{"name":"BIH Center for Regenerative Therapies (BCRT) Charit\u00e9\u2014Universit\u00e4tsmedizin Berlin, corporate member of Freie Universit\u00e4t Berlin, Humboldt\u2014Universit\u00e4t zu Berlin, Berlin Institute of Health Berlin Germany"},{"name":"Institute for Medical Genetics and Human Genetics Charit\u00e9\u2014Universit\u00e4tsmedizin Berlin, corporate member of Freie Universit\u00e4t Berlin, Humboldt\u2014Universit\u00e4t zu Berlin, Berlin Institute of Health Berlin 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