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Serum Phosphate (serum + phosphate)
Terms modified by Serum Phosphate Selected AbstractsFGF23 is a putative marker for bone healing and regenerationJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 9 2009Sascha Goebel Abstract Besides numerous other factors, fibroblast growth factor receptor (FGFR) signaling is involved in fracture healing and bone remodeling. FGF23 is a phosphatonin produced by osteoblastic cells, which signals via FGFR1, thereby exerting effects in bone and kidney. We analyzed if serum FGF23 levels might be an indicator to predict fracture healing and union. FGF23 (C-Term) was elevated on day 3 postoperatively in 55 patients sustaining an exchange of total hip implants due to aseptic loosening. A prospective study of 40 patients undergoing primary hip arthroplasty also showed elevated FGF23 (C-Term) but no change in FGF23 (intact) levels on days 1, 4, and 10 postoperatively. Serum phosphate and phosphate clearance stayed within normal ranges. FGF23 mRNA expression in ovine callus was compared between a standard and delayed course of osteotomy healing. In the standard model, a marked increase in FGF23 mRNA expression compared to the delayed healing situation was observed. Immunohistochemical analysis showed FGF23 production of osteoblasts and granulation tissue in the fracture callus during bone healing. In conclusion, FGF23 is involved in bone healing, can be measured by a sensitive assay in peripheral blood, and is a promising candidate as an indicator for healing processes prone to reunion versus nonunion. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res [source] Alternatives to standard hemodialysisHEMODIALYSIS INTERNATIONAL, Issue 2007Mark S. MACGREGOR Abstract Survival of patients on hemodialysis remains poor, but the benefits of increasing urea clearance have probably been maximized within our current treatment schedules. Long dialysis sessions (8 hr) produce impressive outcomes, with mortality 53% to 55% lower than conventional schedules. Even increasing from 4 to 5 hr may improve survival. Increased frequency of dialysis (6 times weekly) produces impressive reductions in left ventricular mass and could conceivably be implemented in-center. Preliminary data suggest a 61% reduction in mortality with increased frequency. Nightly dialysis combines longer sessions with increased frequency and has produced remarkable clinical gains in blood pressure, left ventricular mass, serum phosphate, and sleep apnea. However, the data are mainly from case series and impact on mortality remains unknown. Expansion of home hemodialysis would be necessary for this modality to grow. Convective therapies remove middle molecules more effectively, and observational data suggest hemodiafiltration has the potential to improve mortality by 35% to 36%. Hemodiafiltration has the advantage of being relatively easy to implement. The uremic milieu is complex and further investigation of the underlying pathophysiology is needed to inform future dialysis interventions. The survival data above are from observational studies, and hence benefits are likely to be exaggerated. Randomized trials of dialysis interventions are desperately needed. They remain difficult to perform, because of the complexity of both the patient population and the interventions, and because of limited available funding. [source] Vitamin D Receptor: Key Roles in Bone Mineral Pathophysiology, Molecular Mechanism of Action, and Novel Nutritional Ligands,JOURNAL OF BONE AND MINERAL RESEARCH, Issue S2 2007Peter W Jurutka Abstract The vitamin D hormone, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], binds with high affinity to the nuclear vitamin D receptor (VDR), which recruits its retinoid X receptor (RXR) heterodimeric partner to recognize vitamin D responsive elements (VDREs) in target genes. 1,25(OH)2D3 is known primarily as a regulator of calcium, but it also controls phosphate (re)absorption at the intestine and kidney. Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone produced in osteoblasts that, like PTH, lowers serum phosphate by inhibiting renal reabsorption through Npt2a/Npt2c. Real-time PCR and reporter gene transfection assays were used to probe VDR-mediated transcriptional control by 1,25(OH)2D3. Reporter gene and mammalian two-hybrid transfections, plus competitive receptor binding assays, were used to discover novel VDR ligands. 1,25(OH)2D3 induces FGF23 78-fold in osteoblasts, and because FGF23 in turn represses 1,25(OH)2D3 synthesis, a reciprocal relationship is established, with FGF23 indirectly curtailing 1,25(OH)2D3 -mediated intestinal absorption and counterbalancing renal reabsorption of phosphate, thereby reversing hyperphosphatemia and preventing ectopic calcification. Therefore, a 1,25(OH)2D3,FGF23 axis regulating phosphate is comparable in importance to the 1,25(OH)2D3,PTH axis that regulates calcium. 1,25(OH)2D3 also elicits regulation of LRP5, Runx2, PHEX, TRPV6, and Npt2c, all anabolic toward bone, and RANKL, which is catabolic. Regulation of mouse RANKL by 1,25(OH)2D3 supports a cloverleaf model, whereby VDR-RXR heterodimers bound to multiple VDREs are juxtapositioned through chromatin looping to form a supercomplex, potentially allowing simultaneous interactions with multiple co-modulators and chromatin remodeling enzymes. VDR also selectively binds certain ,3/,6 polyunsaturated fatty acids (PUFAs) with low affinity, leading to transcriptionally active VDR-RXR complexes. Moreover, the turmeric-derived polyphenol, curcumin, activates transcription of a VDRE reporter construct in human colon cancer cells. Activation of VDR by PUFAs and curcumin may elicit unique, 1,25(OH)2D3 -independent signaling pathways to orchestrate the bioeffects of these lipids in intestine, bone, skin/hair follicle, and other VDR-containing tissues. [source] Regulation of C-Terminal and Intact FGF-23 by Dietary Phosphate in Men and Women,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 8 2006Sherri-Ann M Burnett MD Abstract FGF-23 is a novel regulator of phosphate metabolism. We studied the regulation of FGF-23 by dietary phosphate in 66 men and women using two assays. Dietary phosphate restriction decreased FGF-23 and loading increased FGF-23 significantly. An assay that measured intact FGF-23 showed the effects of dietary phosphate much more clearly than an assay that also measures presumed biologically inactive fragments. Dietary phosphate is a key regulator of circulating FGF-23; choice of assay is critical when studying FGF-23 physiology. Introduction: Fibroblast growth factor 23 (FGF-23) is a novel phosphaturic factor discovered through genetic studies of patients with renal phosphate wasting disorders. Ablation of the FGF-23 gene in mice reduces renal phosphate excretion and increases serum phosphate, suggesting that FGF-23 is critical for normal phosphate homeostasis. We examined the role of dietary phosphate in the regulation of FGF-23 in humans. Materials and Methods: Sixty-six healthy males and females were randomized to either phosphate-depleted or -loaded diets for 5 days, after a 4-day run-in diet. FGF-23 was measured using an "intact" assay that only detects intact FGF-23 peptide and with a "C-terminal" assay that measures both intact FGF-23 peptide and presumed biologically inactive carboxyl terminal fragments. The main outcome was the within group change in FGF-23 with either phosphate depletion or loading. Results: Using the intact FGF-23 assay, mean FGF-23 area under the curve (AUC) decreased by 9 ± 16% with phosphate depletion (p = 0.0041) and increased by 35 ± 29% with loading (p < 0.0001). Using the C-terminal FGF-23 assay, mean FGF-23 AUC decreased by 8 ± 12% with phosphate depletion (p = 0.0003) and increased by 13 ± 20% with loading (p = 0.0016). Increases in FGF-23 with phosphate loading were greater with the intact assay than with the C-terminal assay (p = 0.0003). Using the intact assay only, FGF-23 was significantly associated with serum phosphate (r = 0.39, p < 0.01), 24-h urinary phosphate (r = 0.47, p < 0.01), fractional excretion of phosphate (r = 0.29, p < 0.01), and 1,25-dihydroxyvitamin D (r = ,0.30, p < 0.01). The association between the assays was weak (r = 0.26, p < 0.01). Conclusions: Dietary phosphate is a key regulator of circulating FGF-23 levels in humans. Additionally, choice of assay is critical when performing physiologic investigations of FGF-23. [source] FGF-23 Is a Potent Regulator of Vitamin D Metabolism and Phosphate Homeostasis,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 3 2004Takashi Shimada Abstract We analyzed the effects of an FGF-23 injection in vivo. FGF-23 caused a reduction in serum 1,25-dihydroxyvitamin D by altering the expressions of key enzymes for the vitamin D metabolism followed by hypophosphatemia. This study indicates that FGF-23 is a potent regulator of the vitamin D and phosphate metabolism. Introduction: The pathophysiological contribution of FGF-23 in hypophosphatemic diseases was supported by animal studies in which the long-term administration of recombinant fibroblast growth factor-23 reproduced hypophosphatemic rickets with a low serum 1,25-dihydroxyvitamin D [1,25(OH)2D] level. However, there is no clear understanding of how FGF-23 causes these changes. Materials and Methods: To elucidate the molecular mechanisms of the FGF-23 function, we investigated the short-term effects of a single administration of recombinant FGF-23 in normal and parathyroidectmized animals. Results: An injection of recombinant FGF-23 caused a reduction in serum phosphate and 1,25(OH)2D levels. A decrease in serum phosphate was first observed 9 h after the injection and was accompanied with a reduction in renal mRNA and protein levels for the type IIa sodium-phosphate cotransporter (NaPi-2a). There was no increase in the parathyroid hormone (PTH) level throughout the experiment, and hypophosphatemia was reproduced by FGF-23 in parathyroidectomized rats. Before this hypophosphatemic effect, the serum 1,25(OH)2D level had already descended at 3 h and reached the nadir 9 h after the administration. FGF-23 reduced renal mRNA for 25-hydroxyvitamin D-1,-hydroxylase and increased that for 25-hydroxyvitamin D-24-hydroxylase starting at 1 h. In addition, an injection of calcitriol into normal mice increased the serum FGF-23 level within 4 h. Conclusions: FGF-23 regulates NaPi-2a independently of PTH and the serum 1,25(OH)2D level by controlling renal expressions of key enzymes of the vitamin D metabolism. In conclusion, FGF-23 is a potent regulator of phosphate and vitamin D homeostasis. [source] Age as a predictor of hyperphosphatemia after oral phosphosoda administration for colon preparationJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 1 2004Y GUMURDULU Abstract Background and Aim:, It has been reported that oral phosphosoda (OPS), commonly used in bowel cleansing, may cause complications such as hyperphosphatemia and hypocalcemia. This has been observed in patients with normal kidney function and in those with renal insufficiency. Few controlled studies have been performed with respect to age on healthy subjects after OPS administration. Methods:, Seventy patients (38 men and 32 women; mean age 47 ± 12 years, range 25,80 years) were enrolled in the present study. Half of the 90 mL total volume of OPS was ingested 18 h before colonoscopy, and the other half 6 h before the procedure. Creatinine clearance rate (CCR) and serum levels of sodium, potassium, calcium and phosphate were measured before and after OPS administration. Results:, After OPS administration, serum calcium and potassium were significantly lower (P < 0.05), and serum phosphate and sodium were significantly higher than pretreatment levels (P , 0.01). The statistically significant changes in serum sodium, potassium and calcium were within normal laboratory ranges. The mean change in serum phosphate was positively correlated with age (Pearson's r = 0.705; p < 0.001). Conclusion:, Administration of OPS causes a significant rise in serum phosphate, even in patients with normal CCR. The elevation is significantly greater in elderly patients. Administration of OPS can be considered safe for young and middle-aged patients with normal renal function; however, it should be used with caution in elderly patients, even in those with normal CCR and serum creatinine values. [source] Case,control study of calcification of the hepatic artery in chronic hemodialysis patients: Comparison with the abdominal aorta and splenic arteryJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 1 2002KUNIO OKUDA Abstract Background and Aims: Studies of the hepatic artery are scarce. We have observed that hepatic artery calcification is very uncommon in patients with hyperparathyroidism that expedites calcification. Methods: Plain abdominal CT was studied in 221 patients on chronic hemodialysis. Control consisted of 442 sex- and age-matched patients with other diseases. Calcification was graded as a percentage of the entire wall circumference for the aorta, and as a percentage of the entire length of the hepatic and splenic arteries from the celiac trunk to the hilum of each organ. Results: Aortic calcification was seen in 79.2% of male dialysis patients, 22.1% of controls, 74.1% of female dialysis patients and 17.3% of controls (P < 0.0001). Hepatic artery calcification was seen in only 13 dialysis patients. The degree of calcification of the abdominal aorta was correlated with the length of hemodialysis period (P = 0.008), but not with serum calcium, serum phosphate or their product. Although serum parathormone levels were not correlated with calcification, seven of eight dialysis patients with hepatic artery calcification had very high parathormone levels. Conclusions: The hepatic artery is far less frequently calcified than are the abdominal aorta and splenic artery. This may be a teleologic phenomenon of the liver. [source] EARLY INITIATION OF PHOSPHATE LOWERING DIETARY THERAPY IN NON-DIALYSIS CHRONIC KIDNEY DISEASE: A CRITICAL REVIEWJOURNAL OF RENAL CARE, Issue 2009M.K. Sigrist SUMMARY Dietary management of hyperphosphatemia and hyperparathyroidism have long been important elements in the clinical management of CKD stage 4 and 5 for the prevention of mineral bone disease. The rationale for phosphate lowering has been further justified, given the accumulating data to support the association of phosphate with vascular damage, in this population who are at high risk of cardiovascular (CV) death. Phosphate is a novel CV risk factor in both CKD and in the general population, and a growing body of literature suggests that high normal serum phosphate may be a risk factor for progression of CKD. Few studies have examined hard outcomes after phosphate lowering. Nonetheless, given the balance of data both in cell, animal and human studies, the use of phosphate lowering strategies at earlier stages of CKD, perhaps even prior to serum phosphate level rising, may well be justified. This review will discuss the complications associated with higher serum phosphate, the potential benefits of early phosphate intervention, practical considerations of low phosphate diets and novel strategies for evaluating these strategies in clinical practice. [source] Increased serum phosphate levels and calcium fluxes are seen in smaller individuals after a single dose of sodium phosphate colon cleansing solution: a pharmacokinetic analysisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 11 2009E. D. EHRENPREIS Summary Background, Sodium phosphate containing colonoscopy preparations may cause electrolyte disturbances and calcium-phosphate nephropathy. Decreased body weight is an unexplored risk factor for complications with sodium phosphate ingestion. Aim, To perform a pharmacokinetic analysis of a single dose of Fleet Phospho-Soda in smaller and larger individuals. Methods, Seven subjects weighing <55 kg (Group I) and six weighing >100 kg (Group II) consumed 45 mL Fleet Phospho-Soda. Serum electrolytes were measured. Hydration was closely maintained by monitoring weight, fluid intake and total body water. Results, Marked increases in serum phosphate were seen in Group I compared to Group II. For example, mean serum phosphate at 120 min was 7.8 ± 0.5 mg/dL in Group I and 5.1 ± 0.8 mg/dL in Group II (P < 0.001). Normalized area under the phosphate vs. time curve for Group I was 1120 ± 190 mg/dL*min and 685 ± 136 mg/dL*min for Group II (P < 0.001). Twelve-hour urine calcium was lower in Group I (16.4 ± 7.6 mg) than in Group II (39.2 ± 7.8 mg, P < 0.001). Conclusions, Increased serum phosphate occurs in smaller individuals after ingestion of sodium phosphate preparations, even with strict attention to fluid intake. Smaller body weight poses a potential risk for calcium-phosphate nephropathy. [source] Glomerular toxicity persists 10 years after ifosfamide treatment in childhood and is not predictable by age or dose,PEDIATRIC BLOOD & CANCER, Issue 7 2010FRCPCH, Roderick Skinner PhD Abstract Background This prospective longitudinal single institution cohort study evaluated the natural history of and risk factors for chronic nephrotoxicity 10 years after ifosfamide treatment in childhood. Procedure Twenty-five patients (16 males) treated with ifosfamide were investigated at end of treatment (End), 1 and 10 years later. Glomerular filtration rate (GFR), serum phosphate (PO4) and bicarbonate (HCO3) and renal tubular threshold for phosphate (Tmp/GFR) were measured, and total nephrotoxicity score (Ns) graded. Results More patients had a low GFR at 1 (72%) and 10 (50%) years than at End (26%) (P,=,0.006 for End vs. 1 year). Electrolyte supplementation requirements for tubular toxicity resolved by 10 years (0% vs. 32% at End and 24% at 1 year; both P,<,0.05). At 10 years, 17% of patients had moderate overall nephrotoxicity and 13% clinically significant reduction of GFR (<60,ml/min/1.73,m2). Neither dose nor age at treatment predicted any measure of toxicity at 10 years or reduced GFR at any timepoint. Higher cumulative ifosfamide dose correlated with greater tubular and overall nephrotoxicity at End and/or 1 year (P,<,0.05 for each of PO4, HCO3, Tmp/GFR, Ns), but age at treatment did not differ between patients with normal or abnormal results. Conclusions Although clinically significant tubular toxicity had resolved by 10 years, GFR was <60,ml/min/1.73,m2 in 13% of patients, raising concerns about very long-term glomerular function. Higher cumulative dose was associated with greater tubular and overall toxicity at End and 1 year, but not at 10 years. Age at treatment did not predict nephrotoxicity at any timepoint. Pediatr Blood Cancer 2010;54:983,989 © 2010 Wiley-Liss, Inc. [source] Effects of 0.4 T rotating magnetic field exposure on density, strength, calcium and metabolism of rat thigh bonesBIOELECTROMAGNETICS, Issue 1 2006Xiao-yun Zhang Abstract The current study investigated the effects of 0.4 T rotary non-uniform magnetic field (RMF) exposure on bone density in ovariectomized (OVX) rats. Results showed that many bone indexes are significantly elevated after RMF exposure compared to the control OVX group and confirmed mechanistic evidence that strong magnetic field (MF) exposure could effectively increase bone density and might be used to treat osteoporosis. Synergy of daily RMF exposure (30 min a day for 30 days using an 8 Hz rotary 0.4 T MF) with calcium supplement tended to increase the indexes of thigh bone density, energy absorption, maximum load, maximum flexibility, and elastic deformation as compared to those of untreated OVX control group. Results also revealed that the indexes of alkaline phosphatase (ALP), serum phosphate, and serum calcium were higher in rats exposed to RMF with calcium than in the untreated OVX control group. Changes in bone mineral density (BMD) and bone mineral content (BMC) were observed in rats for three months including the first month RMF exposure. Bone density in rats exposed each day for 60 min increased during 1-month exposure and continued to increase during the post-exposure period. Furthermore, bone density and calcium content in rats exposed for 90 min daily decreased initially in the exposure month; however, ratio of increase was well above the control values by the end of the post-exposure period suggesting possible window and delayed effects. The study indicated that RMF exposure to both male and OVX female rats for 120 min a day over 15 day period should effectively promote increase of bone calcium contents (BCC) and bone-specific alkaline phosphatase (BAP) in rats thigh bone as well as a corresponding decrease in deoxypyridinoline crosslinks (DPD). Bioelectromagnetics 27:1,9, 2006. © 2005 Wiley-Liss, Inc. [source] | |||||||||||||