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Serum Phosphorus (serum + phosphorus)
Terms modified by Serum Phosphorus Selected AbstractsEffect of Iron(III) Chitosan Intake on the Reduction of Serum Phosphorus in RatsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 7 2000JOSEPH BAXTER Because of the widespread use of aluminium- and calcium-containing phosphate binders for the control of hyperphosphataemia in patients with end-stage renal failure, an iron(III) chitosan complex was synthesised and fed to rats to measure its effect on serum phosphorus and calcium, intestinal phosphate binding and phosphate absorption. Thirty-six Wistar rats were randomly selected and distributed into a baseline group (n = 6), a control group (n = 8 (days 0,15), n = 8 (days 16,30)) and a treatment group (n = 8 (days 0,15), n = 8 (days 16,30)). The control groups ingested AIN-76 diet mix with a 1% w/w fibre content; however, the treatment groups had the fibre content completely substituted with iron(III) chitosan. The mean weights of the treated rats were slightly lower from 15 days (not significant); but overall, rat growth was not stunted in the treatment groups. The serum phosphorus levels of the treated group (n = 8) were significantly reduced after 15 days (P = 0.004; control: 5.7 ± 0.9 mg dL,1; treatment: 4.4±0.5 mg dL,1; 95% CI of difference: 0.5,2.2) and 30 days (P = 0.002; control: 5.5 ± 0.9 mg dL,1; treatment = 4.1 ± 0.6 mg dL,1; 95% CI of difference: 0.6,2.3) as compared with the respective control group. The serum calcium-phosphorus product was 62.0 ± 12.1 mg2 dL,2 for the control and 45.1 ± 6.6 mg2 dL,2 for the treatment group after 30 days (P = 0.004). The serum iron concentration of the treatment group did not differ from the baseline value after 15 and 30 days, but the treatment group was significantly higher than the control group (P < 0.05) after 30 days. The faeces phosphorus levels (mg day,1) were higher (P < 0.01) and its iron content was much higher (P < 0.01) for the treated group. The urine phosphorus (mg kg,1) was not significantly reduced for the treated group, but the mean was consistently less. The kidney and liver weights of both groups were similar, but the phosphorus content of the kidney (mg (g kidney),1) was higher for the treated group after 30 days (P = 0.041; control, 4.2 ± 1.2 mg g,1 vs treatment, 5.6 ± 1.4 mg g,1. Because iron(III) chitosan had a high phosphorus-binding capacity of 308 (mg P) per gram of Fe3+ for both the in-vitro (pH 7.5) and in-vivo studies, which is greater than nearly all commonly used phosphate binders, and a small net phosphorus absorption difference of 3.7 mg day,1, it is an efficient phosphate binder for lowering serum phosphate levels without increasing serum calcium levels. [source] Comparison of chronic renal failure rats and modification of the preparation protocol as a hyperphosphataemia modelNEPHROLOGY, Issue 2 2008KAZUHIRO TERAI SUMMARY: Background: Several animal models with chronic renal failure have been established and used for demonstrating complications including hyperphosphataemia. Although long-time feeding is required to cause hyperphosphataemia in animals, a few modifications have been reported to provide more useful models for research. Methods: Three separate experiments were carried out in the present study. First, characteristics of commonly used subnephrectomized (5/6Nx) rats and rats fed an adenine diet (0.75% adenine in normal diet) were compared as hyperphosphataemia models. Next, using adenine-diet rats, the inhibitory effect of sevelamer hydrochloride (Sev) on serum phosphorus elevation was examined. Third, oral adenine dosing for induction of hyperphosphataemia and validation as a model using Sev were examined. Results: Serum phosphorus in 5/6Nx rats became elevated in 8,17 weeks, but the levels and time points of elevation differed among animals. In adenine-fed rats, the elevation was more clearly demonstrated with less diversity at 4 weeks. The data revealed a potential shorter model preparation period and the importance of controlling feeding amounts. Oral adenine dosing induced hyperphosphataemia by 12 days, and Sev treatment was inhibitory. After a maintenance period of over a month (no treatments), Sev-treated rats showed hyperphosphataemia as did oral adenine-dosed control rats. The serum phosphorus levels significantly decreased on further Sev treatment. Conclusion: Oral dosing with adenine made the model preparation period definitely shorter, and its usefulness as a hyperphosphataemia model was revealed using Sev. [source] HMG-CoA reductase inhibitors prevent bone loss in patients with Type 2 diabetes mellitusDIABETIC MEDICINE, Issue 9 2004A. Nakashima Abstract Aims It has been reported that 3-hydroxy-3-methylglutaryl co-enzyme A (HMG-CoA) reductase inhibitors increase bone mineral density (BMD) in vivo. We investigated the effect of HMG-CoA reductase inhibitors on BMD in patients with Type 2 diabetes mellitus. Patients and methods We selected 122 patients with Type 2 diabetes, who were not taking active vitamin D preparations. Their mean age was 67.3 ± 9.2 years. They were divided into a control group (n = 63) without HMG-CoA reductase inhibitor therapy and an HMG-CoA group (n = 59) who were treated with these drugs. The BMD of the distal one-third of the radius was measured by dual-energy X-ray adsorptiometry at baseline and after 2 years. Results There were no significant differences between the control and HMG-CoA groups at baseline with respect to age, gender, body mass index, duration of diabetes, haemoglobin A1c, fasting plasma glucose, adjusted calcium, serum phosphorus, alkaline phosphatase, albumin excretion rate and radial BMD. However, there was a significantly smaller annual decrease of the radial BMD in the HMG-CoA group. Multiple regression analysis with a forward elimination procedure revealed a positive correlation of the radial BMD Z-score with body mass index, while there was a negative correlation with alkaline phosphatase and albumin excretion rate. In addition, the annual rate of change of the radial BMD showed a positive correlation with HMG-CoA reductase inhibitor therapy. Conclusions These findings suggest that HMG-CoA reductase inhibitors may prevent bone loss in patients with Type 2 diabetes. [source] Risk factors of Egyptian male osteoporosisINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 4 2008Salwa S. ELGENDI Abstract Background:, Osteoporosis (OP) is a growing health problem not only in women but also in men. Subjects and methods:, This study was carried out on 100 healthy men, age range 30,65 years (mean ± SD, 44.65 ± 8.3). All were randomly recruited from Assiut city during the period January 2005 to January 2006. Complete clinical history included occupational history, smoking habit, physical activity and calcium intake. Complete clinical examination and anthropometric measurments were done. Laboratory investigations for serum calcium, phosphorus and osteocalcin were performed. Bone mineral density (BMD) was measured by calcaneal ultrasound. Results:, Sixty-three percent of participants had normal BMD, 37% had low BMD, (26% had quantitative bone ultrasound [QUS] T-score ,1 to ,2.5 and 11% had QUS T-score , ,2.5). Smoking and low physical activity were risk factors for low BMD. Significant positive correlations were found between BMD and body mass index, serum calcium, and osteocalcin and negative correlation with phosphorus. We concluded that low BMD occurs with high frequency in Egyptian men. Smoking, physical inactivity and low body index are significant risk factors. Low serum calcium, low serum osteocalcin and high serum phosphorus are biochemical risk factors of low BMD in males. [source] Calcium supplement necessary to correct hypocalcemia after total parathyroidectomy for renal osteodystrophyINTERNATIONAL JOURNAL OF UROLOGY, Issue 2 2000Masayuki Nakagawa Abstract Background: Prediction of the extent of calcium supplement will facilitate safe and efficient management of hypocalcemia in the early postoperative stage of total parathyroidectomy with autotransplantation (PTXa) in patients with renal osteodystrophy. Methods: The correlation between the extent of calcium deficiency, estimated by the amount of calcium supplement over 48 h after PTXa and using various parameters such as carboxy terminal parathyroid hormone (c-PTH), intact PTH (i-PTH), alkaline phosphatase (ALP), serum calcium, serum phosphorus, duration of hemodialysis, total weight of resected parathyroid glands and degree of subperiosteal resorption of the middle phalanx was examined in 49 patients who underwent PTX with subcutaneous autotransplantation. Bone mineral density (BMD) was also determined before, 3 months and 1 year after PTXa with dual energy X-ray absorptiometry (DEXA) in 13 patients. Results: There was a positive correlation between pre-operative i-PTH level (r = 0.56, P < 0.0005) or ALP level (r = 0.50, P < 0.0005) and the amount of calcium supplement over 48 h after PTXa in these patients. Furthermore, the degree of subperiosteal resorption, determined by Jensen's classification, was significantly correlated with the amount of calcium supplement after PTX (P < 0.05). Bone mineral density 3 months after (P < 0.0005) and 1 year after PTXa (P < 0.001) significantly increased compared with BMD before PTXa in all patients examined. Conclusion: These findings suggest that the pre-operative determination of i-PTH, ALP levels and degree of subperiosteal resorption allow the management of hypocalcemia safely and efficiently in renal osteodystrophy patients after PTXa. [source] Effect of Iron(III) Chitosan Intake on the Reduction of Serum Phosphorus in RatsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 7 2000JOSEPH BAXTER Because of the widespread use of aluminium- and calcium-containing phosphate binders for the control of hyperphosphataemia in patients with end-stage renal failure, an iron(III) chitosan complex was synthesised and fed to rats to measure its effect on serum phosphorus and calcium, intestinal phosphate binding and phosphate absorption. Thirty-six Wistar rats were randomly selected and distributed into a baseline group (n = 6), a control group (n = 8 (days 0,15), n = 8 (days 16,30)) and a treatment group (n = 8 (days 0,15), n = 8 (days 16,30)). The control groups ingested AIN-76 diet mix with a 1% w/w fibre content; however, the treatment groups had the fibre content completely substituted with iron(III) chitosan. The mean weights of the treated rats were slightly lower from 15 days (not significant); but overall, rat growth was not stunted in the treatment groups. The serum phosphorus levels of the treated group (n = 8) were significantly reduced after 15 days (P = 0.004; control: 5.7 ± 0.9 mg dL,1; treatment: 4.4±0.5 mg dL,1; 95% CI of difference: 0.5,2.2) and 30 days (P = 0.002; control: 5.5 ± 0.9 mg dL,1; treatment = 4.1 ± 0.6 mg dL,1; 95% CI of difference: 0.6,2.3) as compared with the respective control group. The serum calcium-phosphorus product was 62.0 ± 12.1 mg2 dL,2 for the control and 45.1 ± 6.6 mg2 dL,2 for the treatment group after 30 days (P = 0.004). The serum iron concentration of the treatment group did not differ from the baseline value after 15 and 30 days, but the treatment group was significantly higher than the control group (P < 0.05) after 30 days. The faeces phosphorus levels (mg day,1) were higher (P < 0.01) and its iron content was much higher (P < 0.01) for the treated group. The urine phosphorus (mg kg,1) was not significantly reduced for the treated group, but the mean was consistently less. The kidney and liver weights of both groups were similar, but the phosphorus content of the kidney (mg (g kidney),1) was higher for the treated group after 30 days (P = 0.041; control, 4.2 ± 1.2 mg g,1 vs treatment, 5.6 ± 1.4 mg g,1. Because iron(III) chitosan had a high phosphorus-binding capacity of 308 (mg P) per gram of Fe3+ for both the in-vitro (pH 7.5) and in-vivo studies, which is greater than nearly all commonly used phosphate binders, and a small net phosphorus absorption difference of 3.7 mg day,1, it is an efficient phosphate binder for lowering serum phosphate levels without increasing serum calcium levels. [source] Unrecognized Acute Phosphate Nephropathy in a Kidney Donor with Consequent Poor Allograft OutcomeAMERICAN JOURNAL OF TRANSPLANTATION, Issue 7 2009N. Agrawal Acute phosphate nephropathy following a large phosphate load is a potentially irreversible cause of kidney failure. Here, we report on the unfavorable graft outcome in two recipients of deceased donor kidneys from a donor who had evolving acute phosphate nephropathy at the time of organ procurement. The donor, a 30-year-old with cerebral infarction, developed hypophosphatemia associated with diabetic ketoacidosis and was treated with intravenous phosphate resulting in a rise in serum phosphorus from 0.9 to 6.1 mg/dL. Renal biopsies performed on both recipients for suboptimal kidney function revealed acute tubular injury and diffuse calcium phosphate microcrystal deposits in the tubules, which were persistent in subsequent biopsies. A retrospective review of preimplantation biopsies performed on both kidneys revealed similar findings. Even though initial renal histology in both recipients was negative for BK virus, they eventually developed BK viremia with nephropathy but both had a substantive virologic response with therapy. The first patient returned to dialysis at 6 months, while the other has an estimated glomerular filtration rate of 12 mL/min, 17 months following his transplant. We conclude that unrecognized acute phosphate nephropathy in a deceased donor contributed substantially to poor graft outcome in the two recipients. [source] Effect of treatment with depot somatostatin analogue octreotide on primary hyperparathyroidism (PHP) in multiple endocrine neoplasia type 1 (MEN1) patientsCLINICAL ENDOCRINOLOGY, Issue 5 2008Antongiulio Faggiano Summary Background, In patients with multiple endocrine neoplasia type 1 (MEN1), expression of somatostatin receptor (SST) in parathyroid adenomas and effectiveness of therapy with somatostatin analogues on primary hyperparathyroidism (PHP) have been scarcely investigated. Objective, To evaluate the effects of depot long acting octreotide (OCT-LAR) in patients with MEN1-related PHP. Patients, Eight patients with a genetically confirmed MEN1, presenting both PHP and duodeno-pancreatic neuroendocrine tumours (NET), were enrolled. Design, The initial treatment was OCT-LAR 30 mg every 4 weeks. This therapy was established to stabilize the duodeno-pancreatic NET before to perform parathyroidectomy for PHP. Before OCT-LAR therapy, a SST scintigraphy was performed in all patients. SST subtype 2A immunohistochemistry was performed on parathyroid tumour samples from three patients undergone parathyroidectomy after OCT-LAR therapy. Measurements, Serum concentrations of PTH, calcium and phosphorus as well as the 24-h urine calcium : creatinine ratio and the renal threshold phosphate concentration were evaluated before and after OCT-LAR. Results, After OCT-LAR therapy, hypercalcaemia and hypercalciuria normalized in 75% and 62·5% of patients, respectively, and serum phosphorus and renal threshold phosphate significantly increased. Serum PTH concentrations significantly decreased in all patients and normalized in two of them. SST subtype 2A immunostaining was found in all parathyroid adenomas investigated, while SST scintigraphy showed a positive parathyroid tumour uptake in three of eight patients (37·5%). Conclusion, Six months of OCT-LAR therapy controlled hypercalcaemia and hypercalciuria in two-thirds of patients with MEN1-related PHP. Direct OCT-LAR effects mediated by binding to SST expression on parathyroid tumour cells are likely the main mechanism to explain the activity of this compound on calcium and phosphorus abnormalities in MEN1 PHP. [source] | ||||||||||