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1. Full Text Phenotypic and Genotypic Characterization and Treatment of a Cohort With Familial Tumoral Calcinosis/Hyperostosis‐Hyperphosphatemia Syndrome
by Ramnitz, Mary Scott and Gourh, Pravitt and Goldbach‐Mansky, Raphaela and Wodajo, Felasfa and Ichikawa, Shoji and Econs, Michael J and White, Kenneth E and Molinolo, Alfredo and Chen, Marcus Y and Heller, Theo and Del Rivero, Jaydira and Seo‐Mayer, Patricia and Arabshahi, Bita and Jackson, Malaka B and Hatab, Sarah and McCarthy, Edward and Guthrie, Lori C and Brillante, Beth A and Gafni, Rachel I and Collins, Michael T
Journal of Bone and Mineral Research, ISSN 0884-0431, 10/2016, Volume 31, Issue 10, pp. 1845 - 1854
Familial tumoral calcinosis ( FTC)/hyperostosis-hyperphosphatemia syndrome ( HHS) is a rare disorder caused by mutations in the genes encoding fibroblast... 
FAMILIAL TUMORAL CALCINOSIS | HYPEROSTOSIS‐HYPERPHOSPHATEMIA SYNDROME | FIBROBLAST GROWTH FACTOR 23 | HYPERPHOSPHATEMIA | HYPEROSTOSIS-HYPERPHOSPHATEMIA SYNDROME | GALNT3 | PHOSPHATE BINDER | FIBROBLAST-GROWTH-FACTOR-23 | ACETAZOLAMIDE | HOMOZYGOUS MISSENSE MUTATION | CHILDREN | HYPOPHOSPHATEMIA | ENDOCRINOLOGY & METABOLISM | CALCIFICATION | CALCINOSIS | MANIFESTATIONS | Calcinosis - genetics | Humans | Hyperostosis, Cortical, Congenital - therapy | Fibroblast Growth Factors - genetics | Male | Hyperostosis, Cortical, Congenital - pathology | Hyperphosphatemia - pathology | Hyperphosphatemia - blood | Hyperostosis - blood | N-Acetylgalactosaminyltransferases - genetics | Adult | Female | Hyperostosis - pathology | Hyperphosphatemia - therapy | Child | Hyperostosis - genetics | Hyperostosis - therapy | Calcinosis - blood | Hyperostosis, Cortical, Congenital - genetics | Hyperostosis, Cortical, Congenital - blood | Calcinosis - therapy | Glucuronidase - genetics | Adolescent | Hyperphosphatemia - genetics | Calcinosis - pathology | Cohort Studies | Care and treatment | Phosphorus imbalance | Genetic aspects | C-reactive protein | Gene mutations | Index Medicus | hyperostosis-hyperphosphatemia syndrome | Familial tumoral calcinosis | hyperphosphatemia | fibroblast growth factor 23
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2. Full Text Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease
by Isakova, Tamara and Wahl, Patricia and Vargas, Gabriela S and Gutiérrez, Orlando M and Scialla, Julia and Xie, Huiliang and Appleby, Dina and Nessel, Lisa and Bellovich, Keith and Chen, Jing and Hamm, Lee and Gadegbeku, Crystal and Horwitz, Edward and Townsend, Raymond R and Anderson, Cheryl A.M and Lash, James P and Hsu, Chi-yuan and Leonard, Mary B and Wolf, Myles and on behalf of the Chronic Renal Insufficiency Cohort (CRIC) Study Group and CRIC Study Grp and on behalf of the Chronic Renal Insufficiency Cohort (CRIC) Study Group
Kidney International, ISSN 0085-2538, 06/2011, Volume 79, Issue 12, pp. 1370 - 1378
Fibroblast growth factor 23 (FGF23) regulates phosphorus metabolism and is a strong predictor of mortality in dialysis patients. FGF23 is thought to be an... 
phosphate | FGF23 | chronic kidney disease | MORTALITY | VITAMIN-D | KLOTHO | FIBROBLAST-GROWTH-FACTOR-23 | SECONDARY HYPERPARATHYROIDISM | FGF RECEPTOR | PATHOGENESIS | CALCIUM | UROLOGY & NEPHROLOGY | PHOSPHORUS-METABOLISM | CHRONIC-RENAL-FAILURE | Predictive Value of Tests | Up-Regulation | Biomarkers - urine | Prospective Studies | United States | Humans | Middle Aged | Hyperparathyroidism, Secondary - physiopathology | Male | Parathyroid Hormone - blood | Renal Insufficiency, Chronic - complications | Hyperparathyroidism, Secondary - urine | Hyperphosphatemia - blood | Time Factors | Phosphates - urine | Phosphates - blood | Female | Hyperphosphatemia - urine | Renal Insufficiency, Chronic - diagnosis | Severity of Illness Index | Glomerular Filtration Rate | Phosphorus, Dietary - metabolism | Biomarkers - blood | Renal Insufficiency, Chronic - physiopathology | Renal Insufficiency, Chronic - blood | Hyperparathyroidism, Secondary - blood | Hyperparathyroidism, Secondary - diagnosis | Fibroblast Growth Factors - blood | Hyperphosphatemia - etiology | Aged | Hyperparathyroidism, Secondary - etiology | Hyperphosphatemia - physiopathology | Hyperphosphatemia - diagnosis | Renal Insufficiency, Chronic - urine | Index Medicus
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3. Full Text Use of phosphate-binding agents is associated with a lower risk of mortality
by Cannata-Andía, Jorge B and Fernández-Martín, José L and Locatelli, Francesco and London, Gérard and Gorriz, José L and Floege, Jürgen and Ketteler, Markus and Ferreira, Aníbal and Covic, Adrian and Rutkowski, Boleslaw and Memmos, Dimitrios and Bos, Willem-Jan and Teplan, Vladimir and Nagy, Judit and Tielemans, Christian and Verbeelen, Dierik and Goldsmith, David and Kramar, Reinhard and Martin, Pierre-Yves and Wüthrich, Rudolf P and Pavlovic, Drasko and Benedik, Miha and Sánchez, José Emilio and Martínez-Camblor, Pablo and Naves-Díaz, Manuel and Carrero, Juan J and Zoccali, Carmine
Kidney International, ISSN 0085-2538, 11/2013, Volume 84, Issue 5, pp. 998 - 1008
Hyperphosphatemia has been associated with higher mortality risk in CKD 5 patients receiving dialysis. Here, we determined the association between the use of... 
dialysis | phosphate binders | mineral metabolism | hyperparathyroidism | hyperphosphatemia | mortality risk | VITAMIN-D | EUROPEAN HEMODIALYSIS POPULATION | VASCULAR CALCIFICATION | SECONDARY HYPERPARATHYROIDISM | DIALYSIS PATIENTS | CALCIUM | RENAL-FAILURE | UROLOGY & NEPHROLOGY | CHRONIC KIDNEY-DISEASE | PRACTICE PATTERNS | SEVELAMER HYDROCHLORIDE | Multivariate Analysis | Prospective Studies | Hyperphosphatemia - mortality | Cardiovascular Diseases - prevention & control | Humans | Middle Aged | Male | Hyperphosphatemia - blood | Renal Insufficiency, Chronic - therapy | Renal Dialysis - mortality | Time Factors | Aged, 80 and over | Cardiovascular Diseases - mortality | Phosphates - blood | Renal Insufficiency, Chronic - mortality | Female | Renal Insufficiency, Chronic - diagnosis | Chelating Agents - therapeutic use | Cardiovascular Diseases - diagnosis | Risk Factors | Proportional Hazards Models | Europe - epidemiology | Treatment Outcome | Biomarkers - blood | Chi-Square Distribution | Renal Insufficiency, Chronic - blood | Propensity Score | Renal Dialysis - adverse effects | Hyperphosphatemia - drug therapy | Aged | Hyperphosphatemia - diagnosis | Index Medicus
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4. Full Text Activation of the Nrf2‐ARE Signaling Pathway Prevents Hyperphosphatemia‐Induced Vascular Calcification by Inducing Autophagy in Renal Vascular Smooth Muscle Cells
by Yao, Li and Wang, Jian and Tian, Bin‐Yao and Xu, Tian‐Hua and Sheng, Zi‐Tong
Journal of Cellular Biochemistry, ISSN 0730-2312, 12/2017, Volume 118, Issue 12, pp. 4708 - 4715
Activation of Nrf2‐ARE signaling pathway may prevent hyperphosphatemia‐induced VC by inducing autophagy in VSMCs. 
AUTOPHAGY | HYPERPHOSPHATEMIA‐INDUCED VASCULAR CALCIFICATION | VASCULAR SMOOTH MUSCLE CELL | Nrf2‐ARE SIGNALING PATHWAY | Nrf2-ARE SIGNALING PATHWAY | HYPERPHOSPHATEMIA-INDUCED VASCULAR CALCIFICATION | OXIDATIVE STRESS | MANAGEMENT | INFLAMMATORY DISEASES | BIOCHEMISTRY & MOLECULAR BIOLOGY | SERUM PHOSPHORUS | RUNX2 | CELL BIOLOGY | IN-VITRO | GAMMA-GLUTAMYLCYSTEINE SYNTHETASE | HEMODIALYSIS | CHRONIC KIDNEY-DISEASE | EXPRESSION | Kidney - blood supply | Kidney - pathology | Muscle, Smooth, Vascular - metabolism | Response Elements | Signal Transduction | Myocytes, Smooth Muscle - pathology | Hyperphosphatemia - metabolism | Rats | Vascular Calcification - prevention & control | Male | Vascular Calcification - pathology | Autophagy | Rats, Sprague-Dawley | Hyperphosphatemia - pathology | Vascular Calcification - metabolism | Kidney - metabolism | Muscle, Smooth, Vascular - pathology | Animals | Hyperphosphatemia - prevention & control | NF-E2-Related Factor 2 - metabolism | Myocytes, Smooth Muscle - metabolism | Prevention | Calcification | Smooth muscle | Bone morphogenetic proteins | Phosphorus imbalance | Transmission electron microscopes | Calcification (ectopic) | Cbfa-1 protein | Ion concentration | Kidneys | Bone morphogenetic protein 2 | Calcium | Genes | Phagosomes | Phosphorus | Activation | siRNA | Western blotting | Polymerase chain reaction | Antioxidants | Signal transduction | Biomedical materials | Hyperphosphatemia | Biocompatibility | Phagocytosis | Apoptosis | Index Medicus
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5. Full Text A phase III study of the efficacy and safety of a novel iron-based phosphate binder in dialysis patients
by Floege, Jürgen and Covic, Adrian C and Ketteler, Markus and Rastogi, Anjay and Chong, Edward M.F and Gaillard, Sylvain and Lisk, Laura J and Sprague, Stuart M and PA21 Study Grp and PA21 Study Group
Kidney International, ISSN 0085-2538, 09/2014, Volume 86, Issue 3, pp. 638 - 647
Efficacy of PA21 (sucroferric oxyhydroxide), a novel calcium-free polynuclear iron(III)-oxyhydroxide phosphate binder, was compared with that of sevelamer... 
dialysis | phosphate binder | sevelamer | hyperphosphatemia | PA21 | adherence | MORTALITY | PHOSPHORUS | PREVALENCE | DOPPS | FERRIC CITRATE | HEMODIALYSIS-PATIENTS | UROLOGY & NEPHROLOGY | CHRONIC KIDNEY-DISEASE | PRACTICE PATTERNS | STAGE RENAL-DISEASE | Nausea - chemically induced | Polyamines - adverse effects | Humans | Middle Aged | Induction Chemotherapy | Male | Polyamines - therapeutic use | Patient Dropouts | Renal Insufficiency, Chronic - complications | Diarrhea - chemically induced | Hyperphosphatemia - blood | Renal Insufficiency, Chronic - therapy | Adult | Female | Maintenance Chemotherapy | Sevelamer | Chelating Agents - therapeutic use | Chelating Agents - adverse effects | Constipation - chemically induced | Medication Adherence | Peritoneal Dialysis | Hyperphosphatemia - etiology | Phosphorus - blood | Ferric Compounds - therapeutic use | Hyperphosphatemia - drug therapy | Aged | Ferric Compounds - adverse effects | Index Medicus | Clinical Trial
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6. Full Text Erratum to: Dose–response efficacy and safety of PA21 in Japanese hemodialysis patients with hyperphosphatemia: a randomized, placebo-controlled, double-blind, Phase II study (Clin Exp Nephrol, 10.1007/s10157-016-1299-z)
by Koiwa, Fumihiko and Terao, Akira
Clinical and Experimental Nephrology, ISSN 1342-1751, 06/2017, Volume 21, Issue 3, pp. 523 - 523
To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: http://dx.doi.org/10.1007/s10157-016-1350-0 
Hyperphosphatemia | Hemodialysis
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7. Full Text A randomized trial of JTT-751 versus sevelamer hydrochloride in patients on hemodialysis
by Yokoyama, Keitaro and Akiba, Takashi and Fukagawa, Masafumi and Nakayama, Masaaki and Sawada, Kenichi and Kumagai, Yuji and Chertow, Glenn M and Hirakata, Hideki
Nephrology Dialysis Transplantation, ISSN 0931-0509, 05/2014, Volume 29, Issue 5, pp. 1053 - 1060
Background JTT-751 is a novel phosphate binder containing ferric citrate as the active ingredient. Methods In this Phase 3, multicenter, randomized,... 
hemodialysis | Clinical trial | phosphate binder | ferric citrate | hyperphosphatemia | clinical trial | KIDNEY-DISEASE | DIALYSIS PATIENTS | CALCIUM | KDIGO | UROLOGY & NEPHROLOGY | GUIDELINE | TRANSPLANTATION | Humans | Japan | Middle Aged | Male | Polyamines - therapeutic use | Parathyroid Hormone - blood | Kidney Failure, Chronic - therapy | Young Adult | Hyperphosphatemia - etiology | Ferric Compounds - therapeutic use | Kidney Failure, Chronic - complications | Adult | Female | Hyperphosphatemia - drug therapy | Sevelamer | Chelating Agents - therapeutic use | Hyperphosphatemia - diagnosis | Renal Dialysis | Index Medicus
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8. Full Text Hyperphosphatemia-induced nanocrystals upregulate the expression of bone morphogenetic protein-2 and osteopontin genes in mouse smooth muscle cells in vitro
by Sage, Andrew P and Lu, Jinxiu and Tintut, Yin and Demer, Linda L
Kidney International, ISSN 0085-2538, 02/2011, Volume 79, Issue 4, pp. 414 - 422
Vascular calcification, which contributes to cardiovascular disease in patients with uremic hyperphosphatemia, is associated with vascular cell expression of... 
phosphate | gene transcription | hyperphosphatemia | osteopontin | vascular calcification | EXTRACELLULAR CALCIUM | UREMIC RATS | SERUM | POTENTIAL MECHANISM | MEDIAL CALCIFICATION | CALCIUM-PHOSPHATE CRYSTALS | ARTERIAL CALCIFICATION | UROLOGY & NEPHROLOGY | CHRONIC KIDNEY-DISEASE | FETUIN-A | Osteopontin - genetics | Nanoparticles - chemistry | Myocytes, Smooth Muscle - pathology | Hyperphosphatemia - metabolism | DNA Primers - genetics | Calcinosis - etiology | Base Sequence | Cell Differentiation | Calcinosis - metabolism | Myocytes, Smooth Muscle - drug effects | Myocytes, Smooth Muscle - metabolism | Calcium Phosphates - pharmacology | Osteogenesis - genetics | Hyperphosphatemia - complications | Bone Morphogenetic Protein 2 - genetics | Cell Line | Microscopy, Electron, Scanning | Nanoparticles - ultrastructure | Up-Regulation - drug effects | Animals | Hyperphosphatemia - genetics | Mice | Calcinosis - pathology | In Vitro Techniques | Calcium Phosphates - metabolism | Index Medicus
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9. Full Text Ferric citrate hydrate for the treatment of hyperphosphatemia in nondialysis-dependent CKD
by Yokoyama, Keitaro and Hirakata, Hideki and Akiba, Takashi and Fukagawa, Masafumi and Nakayama, Masaaki and Sawada, Kenichi and Kumagai, Yuji and Block, Geoffrey A
Clinical Journal of the American Society of Nephrology, ISSN 1555-9041, 03/2014, Volume 9, Issue 3, pp. 543 - 552
Background and objectives Ferric citrate hydrate is a novel iron-based phosphate binder being developed for hyperphosphatemia in patients with CKD. Design,... 
PREDIALYSIS PATIENTS | LANTHANUM CARBONATE | CORONARY-ARTERY CALCIFICATION | SERUM PHOSPHATE | GROWTH-FACTOR 23 | RENAL-FAILURE | HEMODIALYSIS-PATIENTS | UROLOGY & NEPHROLOGY | PARATHYROID-HORMONE | MINERAL METABOLISM | CHRONIC KIDNEY-DISEASE | Humans | Middle Aged | Male | Renal Insufficiency, Chronic - complications | Hyperphosphatemia - blood | Ferritins - blood | Time Factors | Phosphates - blood | Female | Renal Insufficiency, Chronic - diagnosis | Chelating Agents - therapeutic use | Chelating Agents - adverse effects | Iron - blood | Double-Blind Method | Japan | Treatment Outcome | Biomarkers - blood | Fibroblast Growth Factors - blood | Hyperphosphatemia - etiology | Ferric Compounds - therapeutic use | Hyperphosphatemia - drug therapy | Aged | Ferric Compounds - adverse effects | Transferrin - metabolism | Hyperphosphatemia - diagnosis | Index Medicus | Original
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10. Full Text Ferric citrate controls phosphorus and delivers iron in patients on dialysis
by Lewis, Julia B and Sika, Mohammed and Koury, Mark J and Chuang, Peale and Schulman, Gerald and Smith, Mark T and Whittier, Frederick C and Linfert, Douglas R and Galphin, Claude M and Athreya, Balaji P and Nossuli, A. Kaldun Kaldun and Chang, Ingrid J and Blumenthal, Samuel S and Manley, John and Zeig, Steven and Kant, Kotagal S and Olivero, Juan Jose and Greene, Tom and Dwyer, Jamie P and Collaborative Study Grp and Collaborative Study Group
Journal of the American Society of Nephrology, ISSN 1046-6673, 02/2015, Volume 26, Issue 2, pp. 493 - 503
Patients on dialysis require phosphorus binders to prevent hyperphosphatemia and are iron deficient. We studied ferric citrate as a phosphorus binder and iron... 
TRIAL | SUPPLEMENTATION | THERAPY | PHOSPHATE BINDER | HYPERPHOSPHATEMIA | ELEVATED FERRITIN | HIGH SERUM FERRITIN | HEMODIALYSIS-PATIENTS | UROLOGY & NEPHROLOGY | ANEMIA | CHRONIC KIDNEY-DISEASE | Outcome Assessment (Health Care) | United States | Humans | Middle Aged | Hyperphosphatemia - metabolism | Male | Treatment Outcome | Anemia, Iron-Deficiency - prevention & control | Iron - metabolism | Kidney Failure, Chronic - metabolism | Dose-Response Relationship, Drug | Kidney Failure, Chronic - therapy | Hyperphosphatemia - prevention & control | Phosphorus - metabolism | Ferric Compounds - therapeutic use | Female | Israel | Anemia, Iron-Deficiency - metabolism | Renal Dialysis | Index Medicus | clinical trial | dialysis | phosphate binders | Clinical Research | anemia
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11. Full Text Initiation of sevelamer and mortality among hemodialysis patients treated with calcium-based phosphate binders
by Komaba, Hirotaka and Wang, Mia and Taniguchi, Masatomo and Yamamoto, Suguru and Nomura, Takanobu and Schaubel, Douglas E and Smith, Abigail R and Zee, Jarcy and Karaboyas, Angelo and Bieber, Brian and Fukagawa, Masafumi and Tentori, Francesca
Clinical Journal of the American Society of Nephrology, ISSN 1555-9041, 09/2017, Volume 12, Issue 9, pp. 1489 - 1497
Background and objectives Prior studies have shown that sevelamer attenuates progression of arterial calcification and may reduce the risk of death compared... 
CORONARY-ARTERY CALCIFICATION | SERUM PHOSPHATE | PROPENSITY SCORE | NUTRITIONAL-STATUS | DIALYSIS OUTCOMES | UROLOGY & NEPHROLOGY | MINERAL METABOLISM | DOPPS | PRACTICE PATTERNS | CKD | HYDROCHLORIDE | Prospective Studies | Hyperphosphatemia - mortality | Humans | Middle Aged | Male | Practice Patterns, Physicians | North America | Sevelamer - therapeutic use | Hyperphosphatemia - blood | Renal Insufficiency, Chronic - therapy | Kidney - metabolism | Renal Dialysis - mortality | Time Factors | Phosphates - blood | Renal Insufficiency, Chronic - mortality | Female | Drug Therapy, Combination | Sevelamer - adverse effects | Chelating Agents - therapeutic use | Kidney - physiopathology | Chelating Agents - adverse effects | Kidney - drug effects | Europe | Risk Factors | Proportional Hazards Models | Treatment Outcome | Biomarkers - blood | Renal Insufficiency, Chronic - physiopathology | New Zealand | Renal Insufficiency, Chronic - blood | Propensity Score | Renal Dialysis - adverse effects | Hyperphosphatemia - drug therapy | Aged | Australia | Drug Substitution | Hyperphosphatemia - physiopathology | Health Care Surveys | Index Medicus | Fluid Therapy | Confidence Intervals | Calcium, Dietary | Dialysis Outcomes and Practice Patterns Study (DOPPS): hemodialysis | survival | sevelamer | Phosphorus | Calcium Phosphates | hyperphosphatemia | calcium phosphate | Original | renal dialysis
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12. Full Text Gitelman's syndrome with hyperphosphatemia, effectively responding to single oral magnesium oxide administration: A case report
by Miya, Aika and Nakamura, Akinobu and Kameda, Hiraku and Nozu, Kandai and Miyoshi, Hideaki and Atsumi, Tatsuya
Medicine, ISSN 0025-7974, 07/2019, Volume 98, Issue 28, pp. e16408 - e16408
The Gitelman's syndrome (GS) is characterized by metabolic alkalosis, hypokalemia, hypomagnesemia, and hypocalciuria. However, the involvement of this deranged... 
Antacids - therapeutic use | Hyperphosphatemia - complications | Gitelman Syndrome - drug therapy | Administration, Oral | Magnesium Oxide - therapeutic use | Humans | Gitelman Syndrome - complications | Adult | Female | Hyperphosphatemia - drug therapy | Hyperphosphatemia - genetics | Gitelman Syndrome - genetics | parathyroid hormone | MEDICINE, GENERAL & INTERNAL | HORMONE | hyperphosphatemia | DISEASE | hypomagnesemia | COTRANSPORTER GENE | Gitelman's syndrome | MUTATIONS | hypocalciuric hypocalcemia | BARTTERS-SYNDROME | Case studies | Usage | Genetic disorders | Magnesium oxide | Phosphorus imbalance | Kidney diseases | Drug therapy
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