Database : MEDLINE
Search on : Hyperphosphatemia [Words]
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[PMID]: 29523679
[Au] Autor:Lau WL; Obi Y; Kalantar-Zadeh K
[Ad] Address:Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California, Irvine, California.
[Ti] Title:Parathyroidectomy in the Management of Secondary Hyperparathyroidism.
[So] Source:Clin J Am Soc Nephrol;, 2018 Mar 09.
[Is] ISSN:1555-905X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Secondary hyperparathyroidism develops in CKD due to a combination of vitamin D deficiency, hypocalcemia, and hyperphosphatemia, and it exists in nearly all patients at the time of dialysis initiation. There is insufficient data on whether to prefer vitamin D analogs compared with calcimimetics, but the available evidence suggests advantages with combination therapy. Calcium derangements, patient adherence, side effects, and cost limit the use of these agents. When parathyroid hormone level persists >800 pg/ml for >6 months, despite exhaustive medical interventions, monoclonal proliferation with nodular hyperplasia is likely present along with decreased expression of vitamin D and calcium-sensing receptors. Hence, surgical parathyroidectomy should be considered, especially if concomitant disorders exist, such as persistent hypercalcemia or hyperphosphatemia, tissue or vascular calcification including calciphylaxis, and/or worsening osteodystrophy. Parathyroidectomy is associated with 15%-57% greater survival in patients on dialysis, and it also improves hypercalcemia, hyperphosphatemia, tissue calcification, bone mineral density, and health-related quality of life. The parathyroidectomy rate in the United States declined to approximately seven per 1000 dialysis patient-years between 2002 and 2011 despite an increase in average parathyroid hormone levels, reflecting calcimimetics introduction and uncertainty regarding optimal parathyroid hormone targets. Hospitalization rates are 39% higher in the first postoperative year. Hungry bone syndrome occurs in approximately 25% of patients on dialysis, and profound hypocalcemia requires high doses of oral and intravenous calcium along with calcitriol supplementation. Total parathyroidectomy with autotransplantation carries a higher risk of permanent hypocalcemia, whereas risk of hyperparathyroidism recurrence is higher with subtotal parathyroidectomy. Given favorable long-term outcomes from observational parathyroidectomy cohorts, despite surgical risk and postoperative challenges, it is reasonable to consider parathyroidectomy in more patients with medically refractory secondary hyperparathyroidism.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 3375 MEDLINE  
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[PMID]: 29519353
[Au] Autor:Kranenburg G; de Jong PA; Bartstra JW; Lagerweij SJ; Lam MG; Ossewaarde-van Norel J; Risseeuw S; van Leeuwen R; Imhof SM; Verhaar HJ; de Vries JJ; Slart RHJA; Luurtsema G; den Harder AM; Visseren FLJ; Mali WP; Spiering W
[Ad] Address:Department of Vascular Medicine, University Medical Center Utrecht, Utrecht University, Utrecht, the Netherlands.
[Ti] Title:Etidronate for Prevention of Ectopic Mineralization in Patients With Pseudoxanthoma Elasticum.
[So] Source:J Am Coll Cardiol;71(10):1117-1126, 2018 Mar 13.
[Is] ISSN:1558-3597
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: In pseudoxanthoma elasticum (PXE), low pyrophosphate levels may cause ectopic mineralization, leading to skin changes, visual impairment, and peripheral arterial disease. OBJECTIVES: The authors hypothesized that etidronate, a pyrophosphate analog, might reduce ectopic mineralization in PXE. METHODS: In the Treatment of Ectopic Mineralization in Pseudoxanthoma Elasticum trial, adults with PXE and leg arterial calcifications (n = 74) were randomly assigned to etidronate or placebo (cyclical 20 mg/kg for 2 weeks every 12 weeks). The primary outcome was ectopic mineralization, quantified with fluoride positron emission tomography scans as femoral arterial wall target-to-background ratios (TBR ). Secondary outcomes were computed tomography arterial calcification and ophthalmological changes. Safety outcomes were bone density, serum calcium, and phosphate. RESULTS: During 12 months of follow-up, the TBR increased 6% (interquartile range [IQR]: -12% to 25%) in the etidronate group and 7% (IQR: -9% to 32%) in the placebo group (p = 0.465). Arterial calcification decreased 4% (IQR: -11% to 7%) in the etidronate group and increased 8% (IQR: -1% to 20%) in the placebo group (p = 0.001). Etidronate treatment was associated with significantly fewer subretinal neovascularization events (1 vs. 9, p = 0.007). Bone density decreased 4% ± 12% in the etidronate group and 6% ± 9% in the placebo group (p = 0.374). Hypocalcemia (<2.20 mmol/l) occurred in 3 versus 1 patient (8.1% vs. 2.7%, p = 0.304). Eighteen patients (48.6%) treated with etidronate, compared with 0 patients treated with placebo (p < 0.001), experienced hyperphosphatemia (>1.5 mmol/l) and recovered spontaneously. CONCLUSIONS: In patients with PXE, etidronate reduced arterial calcification and subretinal neovascularization events but did not lower femoral fluoride sodium positron emission tomography activity compared with placebo, without important safety issues. (Treatment of Ectopic Mineralization in Pseudoxanthoma elasticum; NTR5180).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  3 / 3375 MEDLINE  
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[PMID]: 29519205
[Au] Autor:Miller CJ; Doepker BA; Springer AN; Exline MC; Phillips G; Murphy CV
[Ad] Address:1 Department of Pharmacy, University of Colorado Hospital, Aurora, CO, USA.
[Ti] Title:Impact of Serum Phosphate in Mechanically Ventilated Patients With Severe Sepsis and Septic Shock.
[So] Source:J Intensive Care Med;:885066618762753, 2018 Jan 01.
[Is] ISSN:1525-1489
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Hypo- and hyperphosphatemia are common in severe sepsis and septic shock. Published outcome data in patients with phosphate derangements primarily focus on hypophosphatemia and the general critically ill population. This study aimed to determine the impact of serum phosphate on clinical outcomes in patients with severe sepsis and septic shock. METHODS: A retrospective cohort analysis of adult mechanically ventilated patients with severe sepsis or septic shock was performed. Patients were randomly selected from an internal intensive care unit (ICU) database at an academic medical center in the United States and screened for inclusion and exclusion criteria. Time-weighted phosphate was calculated using all phosphate measurements obtained during ICU admission. The associations between time-weighted phosphate and duration of mechanical ventilation, 28-day mortality, and ICU and hospital length of stay were evaluated using linear or logistic regression as appropriate. RESULTS: One-hundred ninety-seven patients were evaluated: 33 were categorized as hypophosphatemia, 123 as normophosphatemia, and 41 as hyperphosphatemia. Patients with time-weighted hyperphosphatemia had a higher Simplified Acute Physiology Score III score and incidence of septic shock. Significantly higher rates of 28-day mortality were observed among those with time-weighted phosphate levels above 3.5 mg/dL. However, both time-weighted hypo- and hyperphosphatemia were associated with decreased duration of mechanical ventilation. For every 0.5 mg/dL increase in time-weighted phosphate referent values from 4.0 to 6.0, the duration of mechanical ventilation decreased by 8% to 26%. For every 0.5 mg/dL decrease in time-weighted phosphate referent values from 3.0 to 1.0, significant decreases in duration of mechanical ventilation ranged from 14% to 41%. CONCLUSION: Time-weighted hyperphosphatemia may be associated with increased mortality in mechanically ventilated patients with severe sepsis or septic shock. However, time-weighted hypo- and hyperphosphatemia were associated with decreased duration of mechanical ventilation. Future studies should further describe the impact of hypo- and hyperphosphatemia on clinical outcomes among critically ill patients with severe sepsis or septic shock.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1177/0885066618762753

  4 / 3375 MEDLINE  
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[PMID]: 29489687
[Au] Autor:Li L; Yang H; Li J; Yu Y; Wang F; Zhu X; Liu G
[Ad] Address:Department of Neurology, PLA 44 Hospital.
[Ti] Title:Misdiagnosis of idiopathic hypoparathyroidism: A case report and literature review.
[So] Source:Medicine (Baltimore);97(9):e9884, 2018 Mar.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Idiopathic hypoparathyroidism (IHP) is a rare endocrine condition, which is frequently represented by neuropsychiatric disorders. Hence, the misdiagnosis rate of the disease is rather high, especially for neurologists. PATIENT CONCERNS: We reported a case of misdiagnosed, atypical IHP. In addition, the literature on IHP and the misdiagnosis published in China in the past 2 decades has been reviewed and summarized. DIAGNOSES: Blood testing confirmed that parathyroid hormone (PTH) = 0 pg/mL and the final diagnosis was IHP. INTERVENTIONS AND OUTCOMES: With calcium and vitamin D supplementation, the patient's myasthenia improved significantly, and muscle enzymes returned to normal gradually. One-year follow-up demonstrated that the patient's myasthenia disappeared, and the blood calcium and PTH levels were normal. In addition, the literature on IHP and the misdiagnosis published in China in the past 2 decades has been reviewed and summarized. LESSONS: The misdiagnosis rate of IHP in China was high in the past 2 decades, which might be attributed to the misdiagnosis as epilepsy or mental diseases. A clinician should be able to understand the disease and emphasize the screening of high-risk population, especially for those patients with hypocalcemia, hyperphosphatemia, and increased blood creatine kinase with unknown causes or nontypical clinical symptoms.
[Mh] MeSH terms primary: Diagnostic Errors/adverse effects
Hypoparathyroidism/diagnosis
[Mh] MeSH terms secundary: Adult
Female
Humans
Hypoparathyroidism/drug therapy
Parathyroid Hormone/blood
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Parathyroid Hormone)
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180301
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009884

  5 / 3375 MEDLINE  
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[PMID]: 29309658
[Au] Autor:Neuburg S; Dussold C; Gerber C; Wang X; Francis C; Qi L; David V; Wolf M; Martin A
[Ad] Address:Division of Nephrology and Hypertension, Department of Medicine, Center for Translational Metabolism and Health, Institute for Public Health and Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
[Ti] Title:Genetic background influences cardiac phenotype in murine chronic kidney disease.
[So] Source:Nephrol Dial Transplant;, 2017 Dec 22.
[Is] ISSN:1460-2385
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: Levels of fibroblast growth factor 23 (FGF23) increase early in chronic kidney disease (CKD) and are independently associated with left ventricular hypertrophy (LVH), heart failure and death. Experimental models of CKD with elevated FGF23 and LVH are needed. We hypothesized that slow rates of CKD progression in the Col4a3 knockout (Col4a3KO) mouse model of CKD would promote development of LVH by prolonging exposure to elevated FGF23. Methods: We studied congenic Col4a3KO and wild-type (WT) mice with either 75% 129X1/SvJ (129Sv) or 94% C57Bl6/J (B6) genomes. Results: B6-Col4a3KO lived longer than 129Sv-Col4a3KO mice (21.4 ± 0.6 versus 11.4 ± 0.4 weeks; P < 0.05). 10-week-old 129Sv-Col4a3KO mice showed impaired renal function (blood urea nitrogen 191 ± 39 versus 34 ± 4 mg/dL), hyperphosphatemia (14.1 ± 1.4 versus 6.8 ± 0.3 mg/dL) and 33-fold higher serum FGF23 levels (P < 0.05 versus WT for each). Consistent with their slower CKD progression, 10 week-old B6-Col4a3KO mice showed milder impairment of renal function than 129Sv-Col4a3KO mice and modest FGF23 elevation without other alterations of mineral metabolism. At 20 weeks, further declines in renal function in B6-Col4a3KO mice was accompanied by hyperphosphatemia and 8-fold higher FGF23 levels (P < 0.05 versus WT for each). Only the 20-week-old B6-Col4a3KO mice developed LVH (LV mass 125 ± 3 versus 98 ± 6 mg; P < 0.05 versus WT) in association with significantly increased cardiac expression of FGF receptor 4 (FGFR4) messenger RNA and protein and markers of LVH (Atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), beta-myosin heavy chain (ß-MHC); P < 0.05 versus WT for each). Conclusions: n conclusion, B6-Col4a3KO mice manifest slower CKD progression and longer survival than 129Sv-Col4a3KO mice and can serve as a novel model of cardiorenal disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/ndt/gfx332

  6 / 3375 MEDLINE  
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[PMID]: 29486729
[Au] Autor:Zhang YY; Yang M; Bao JF; Gu LJ; Yu HL; Yuan WJ
[Ad] Address:Department of Nephrology, Shanghai General Hospital, Shanghai Jiaotong University School of Medcine, Haining Road 100rd, Hongkou Distrinct, Shanghai, 200080, China.
[Ti] Title:Phosphate stimulates myotube atrophy through autophagy activation: evidence of hyperphosphatemia contributing to skeletal muscle wasting in chronic kidney disease.
[So] Source:BMC Nephrol;19(1):45, 2018 Feb 27.
[Is] ISSN:1471-2369
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Accelerated muscle atrophy is associated with a three-fold increase in mortality in chronic kidney disease (CKD) patients. It is suggested that hyperphosphatemia might contribute to muscle wasting, but the underlying mechanisms remain unclear. Although evidence indicates that autophagy is involved in the maintenance of muscle homeostasis, it is not known if high phosphate levels can result in activation of autophagy, leading to muscle protein loss. METHODS: Immortalized rat L6 myotubes were exposed to a high concentration of phosphate, with or without autophagy inhibition. Myotube atrophy was examined by phase contrast microscopy. Autophagic activity was assessed by measuring the expression of microtubule-associated protein 1 light chain 3 (LC3) and p62 using quantitative real-time polymerase chain reaction and western blot. RESULTS: Phosphate induced cell atrophy in L6 myotubes in a dose- and time-dependent manner, and these responses were not associated with calcification or osteogenesis. Phosphate also dose- and time-dependently increased the LC3-II/LC3-I ratio. Inhibition of autophagy with wortmannin or knockdown of Atg5 significantly suppressed myotube atrophy caused by high phosphate concentration. CONCLUSIONS: High phosphate concentration induces muscle cell atrophy through the activation of autophagy. Targeting autophagy could be a therapeutic strategy for preventing muscle wasting caused by hyperphosphatemia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1186/s12882-018-0836-2

  7 / 3375 MEDLINE  
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[PMID]: 28464802
[Au] Autor:Neradova A; Schumacher SP; Hubeek I; Lux P; Schurgers LJ; Vervloet MG
[Ad] Address:Department of Nephrology, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. a.neradova@vumc.nl.
[Ti] Title:Phosphate binders affect vitamin K concentration by undesired binding, an in vitro study.
[So] Source:BMC Nephrol;18(1):149, 2017 May 02.
[Is] ISSN:1471-2369
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Vascular calcification is a major contributing factor to mortality in end stage renal disease (ESRD). Despite the efficacy of phosphate binders to improve hyperphosphatemia, data on vascular calcification are less clear. There seems to be a difference in attenuation or delay in progression between different binders. In this in vitro experiment we tested whether phosphate binders could limit bioavailability of vitamin K2 by undesired binding. Vitamin K-deficiency limits activation of the vascular tissue mineralization inhibitor matrix γ-carboxyglutamate (Gla) protein (MGP) thereby exacerbating vascular calcification. METHODS: In this experiment vitamin K2 (menaquinone-7; MK-7) binding was assessed by adding 1 mg of vitamin K2 to a medium with pH 6 containing 67 mg phosphate binder with either 7 mg of phosphate or no phosphate. Five different phosphate binders were tested. After five and a half hours vitamin K was analyzed by HPLC. All experiments were performed in triplicate. RESULTS: Sucroferric-oxyhydroxide and sevelamer carbonate did not significantly bind vitamin K2, both in solution only containing vitamin K2 or in combination with phosphate. Calcium acetate/magnesium carbonate binds vitamin K2 strongly both in absence (p = 0.001) and presence of phosphate (p = 0.003). Lanthanum carbonate significantly binds vitamin K2 in solution containing only vitamin K2 (p = 0.005) whereas no significant binding of vitamin K2 was observed in the solution containing vitamin K2 and phosphate (p = 0.462). Calcium carbonate binds vitamin K2 significantly in a solution with vitamin K2 and phosphate (p = 0.009) whereas without phosphate no significant binding of vitamin K2 was observed (p = 0.123). CONCLUSIONS: Sucroferric-oxyhydroxide and sevelamer carbonate were the only binders of the five binders studied that did not bind vitamin K2 in vitro. The presence or absence of phosphate significantly interferes with vitamin K2 binding so phosphate binders could potentially limit bioavailability vitamin K2.
[Mh] MeSH terms primary: Chelating Agents/chemistry
Phosphates/chemistry
Vitamin K/chemistry
[Mh] MeSH terms secundary: Protein Binding
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Chelating Agents); 0 (Phosphates); 12001-79-5 (Vitamin K)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:IM
[Da] Date of entry for processing:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12882-017-0560-3

  8 / 3375 MEDLINE  
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[PMID]: 29494340
[Au] Autor:Ajarmeh SA; Al Tamimi EM
[Ad] Address:Department of Pediatrics, Faculty of Medicine, Mutah University, 61710 Karak, Jordan.
[Ti] Title:Sanjad-Sakati syndrome with macrocytic anemia and failure to thrive: a case from South Jordan.
[So] Source:J Pediatr Endocrinol Metab;, 2018 Mar 01.
[Is] ISSN:2191-0251
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Backgorund: Sanjad-Sakati syndrome (SSS) is a rare autosomal recessive disease caused by a deletion mutation (155-166del) in exon 3 of the TBCE gene on chromosome 1q42-43. The syndrome is characterized by primary hypoparathyroidism, typical dysmorphic features and severe growth retardation. CASE PRESENTATION: We encountered a 2-year-old boy with hypocalcemia, failure to thrive and macrocytic anemia. The patient had the characteristic features of SSS and genetic testing confirmed that he was homozygous for the TBCE mutation. Although malabsorption was initially considered the cause of his symptoms, the results did not confirm that diagnosis. Our patient had cow milk protein allergy and folic acid deficiency, which has not been described in previous SSS cases. It was difficult to treat the patient's hyperphosphatemia and we ultimately selected sevelamer treatment, which was tolerated well and improved his hypocalcemia. CONCLUSIONS: SSS should be considered in the differential diagnosis of any infant with hypocalcemia, dysmorphism and failure to thrive.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:Publisher

  9 / 3375 MEDLINE  
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[PMID]: 29493868
[Au] Autor:Brønden A; Mikkelsen K; Sonne DP; Hansen M; Våben C; Gabe MN; Rosenkilde M; Tremaroli V; Wu H; Bäckhed F; Rehfeld JF; Holst JJ; Vilsbøll T; Knop FK
[Ad] Address:Center for Diabetes Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
[Ti] Title:Glucose-lowering effects and mechanisms of the bile acid-sequestering resin sevelamer.
[So] Source:Diabetes Obes Metab;, 2018 Mar 01.
[Is] ISSN:1463-1326
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:AIMS: Sevelamer, a non-absorbable amine-based resin used for treatment of hyperphosphatemia, has been demonstrated to hold a marked bile acid-binding potential alongside beneficial effects on lipid and glucose metabolism. The aim of this study was to investigate the glucose-lowering effect and mechanism(s) of sevelamer in patients with type 2 diabetes. MATERIALS AND METHODS: In this double-blinded randomized controlled trial, we randomized 30 patients with type 2 diabetes to sevelamer (n=20) or placebo (n=10). Participants were subjected to standardized 4-hour liquid meal tests at baseline and following seven days of treatment. The main outcome measure was plasma glucagon-like peptide-1 excursions as measured by area under the curve. In addition, blood was sampled for measurements of glucose, lipids, glucose-dependent insulinotropic polypeptide, C-peptide, glucagon, fibroblast growth factor-19, cholecystokinin and bile acids. Assessments of gastric emptying, resting energy expenditure and gut microbiota composition were performed. RESULTS: Sevelamer elicited a significant placebo-corrected reduction in plasma glucose with concomitant reduced fibroblast growth factor-19 concentrations, increased de novo synthesis of bile acids, a shift towards a more hydrophilic bile acid pool and increased lipogenesis. No glucagon-like peptide-1-mediated effects on insulin, glucagon or gastric emptying were evident, which point to limited contribution of this incretin hormone to the glucose-lowering effect of sevelamer. Furthermore, no sevelamer-mediated effects on gut microbiota composition or resting energy expenditure were observed. CONCLUSIONS: Sevelamer reduced plasma glucose concentrations in patients with type 2 diabetes by mechanisms that seemed to involve decreased intestinal and hepatic bile acid-mediated farnesoid X receptor activation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:Publisher
[do] DOI:10.1111/dom.13272

  10 / 3375 MEDLINE  
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[PMID]: 29415048
[Au] Autor:Jung SY; Kwon J; Park S; Jhee JH; Yun HR; Kim H; Kee YK; Yoon CY; Chang TI; Kang EW; Park JT; Yoo TH; Kang SW; Han SH
[Ad] Address:Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea.
[Ti] Title:Phosphate is a potential biomarker of disease severity and predicts adverse outcomes in acute kidney injury patients undergoing continuous renal replacement therapy.
[So] Source:PLoS One;13(2):e0191290, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hyperphosphatemia is associated with mortality in patients with chronic kidney disease, and is common in critically ill patients with acute kidney injury (AKI); however, its clinical implication in these patients is unknown. We conducted an observational study in 1144 patients (mean age, 63.2 years; male, 705 [61.6%]) with AKI who received continuous renal replacement therapy (CRRT) between January 2009 and September 2016. Phosphate levels were measured before (0 h) and 24 h after CRRT initiation. We assessed disease severity using various clinical parameters. Phosphate at 0 h positively correlated with the Acute Physiology and Chronic Health Evaluation II (APACHE II; P < 0.001) and Sequential Organ Failure Assessment (SOFA; P < 0.001) scores, and inversely with mean arterial pressure (MAP; P = 0.02) and urine output (UO; P = 0.01). In a fully adjusted linear regression analysis for age, sex, Charlson comorbidity index (CCI), MAP, and estimated glomerular filtration rate (eGFR), higher 0 h phosphate level was significantly associated with high APACHE II (P < 0.001) and SOFA (P = 0.04) scores, suggesting that phosphate represents disease severity. A multivariable Cox model also showed that hyperphosphatemia was significantly associated with increased 28-day (HR 1.05, 95% CI 1.02-1.08, P = 0.001) and 90-day (HR 1.05, 95% CI 1.02-1.08, P = 0.001) mortality. Furthermore, patients with increased phosphate level during 24 h were at higher risk of death than those with stable or decreased phosphate levels. Finally, c-statistics significantly increased when phosphate was added to a model that included age, sex, CCI, body mass index, eGFR, MAP, hemoglobin, serum albumin, C-reactive protein, and APACHE II score. This study shows that phosphate is a potential biomarker that can reflect disease severity and predict mortality in critically ill patients receiving CRRT.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:In-Process
[do] DOI:10.1371/journal.pone.0191290


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