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(2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Renal proximal tubule and systemic mineral phenotype","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"8a3d2400-0727-50ed-a7c3-679bafc810c6","evidence_kind":"source_excerpt","locator":"Lines 694-705","start_line":694,"end_line":705,"excerpt":"### sodium-napi2c-calcium\nThe sodium/phosphate-transporter-associated HHRH phenotype included hypercalciuria.\nCondition category: machinery_impairment\nnutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: This phosphate disorder can also increase calcium loss into urine.\norganism: Human\ntissue_or_cell_type: Renal proximal tubule and systemic mineral phenotype\nexperimental_model: Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria\nlimitations: Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention.\nexposure: SLC34A3 disease-associated mutations in five families\nevidence_span: {\"source_cache\": \"artifacts/sodium-research/16358215.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb\", \"start_char\": 0, \"end_char\": 1515, \"text_sha256\": \"876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb\"}\n[sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. 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