碳酸镧治疗维持性血液透析患者高磷血症的临床疗效

目的 探讨碳酸镧治疗维持性血液透析患者高磷血症的疗效.方法 选择2014年1月至2015年12月在连云港市第一人民医院维持性血液透析的50例患者为研究对象(透析至少6个月),随机分为碳酸镧组(LC组)和碳酸钙组(CC组),每组各25例,治疗4周、24周后,分别比较两组治疗前后血磷、血钙、甲状旁腺激素水平,24周后两组间钙、磷、甲状旁腺激素水平.结果 47例患者完成治疗及随访.与治疗前相比,两组患者治疗4周后的血磷水平均下降,差异有统计学意义(P＜0.05);与治疗前相比,两组患者治疗24周后的血磷水平下降,差异有统计学意义(P＜0.05).LC组整个治疗过程中血钙无明显变化,差异无统计学意义(P＞0.05),而CC组治疗24周后血钙水平升高,差异有统计学意义(P＜0.05).两组患者的甲状旁腺激素水平较治疗前下降,差异有统计学意义(P＜0.05).治疗24周后,LC组患者血磷、血钙、甲状旁腺激素水平低于CC组,差异有统计学意义(P＜0.05).结论 碳酸镧能安全有效治疗终末期肾衰透析患者高磷血症,降磷作用持久、副作用少,且更安全有效.     

氯霉素对EBPR系统除磷性能的影响及其机制

目的 探究氯霉素(chloramphenicol，CAP)(0.01~3mmol/L)对强化生物除磷(EBPR)系统除磷性能的影响及其机制。方法 采用活性污泥构建EBPR系统，测定CAP对该系统除磷性能的影响，分析CAP对聚磷菌(polyphosphate accumulating organisms，PAOs)代谢中间产物(聚羟基烷酸酯、糖原)代谢及关键酶(多聚磷酸盐激酶、多聚磷酸盐酯酶和腺苷酸激酶)活性的影响。结果 0.01~3mmol/L CAP对EBPR系统的除磷抑制率介于-6.08%~100%。较高浓度的CAP(≥1mmol/L)可破坏好氧阶段聚羟基烷酸酯与糖原的正常代谢(P<0.05)，对除磷关键酶活性也存在不同程度的显著抑制(P<0.05)。结论 CAP(0.3~3mmol/L)可影响EBPR系统中PAOs体内好氧段聚羟基烷酸酯及糖原的代谢及抑制除磷关键酶的活性，使得系统的除磷性能减弱，低浓度(0~0.1mmol/L)CAP对EBPR系统无明显不利影响。     

Effects of Race on Diurnal Patterns of Renal Conservation of Calcium and Bone Resorption in Premenopausal Women

Previous studies showed differences in bone and mineral metabolism in African-Americans and Caucasians: reductions in serum 25-hydroxyvitamin D [25(OH)D], urinary calcium and skeletal remodeling and moderate secondary hyperparathyroidism. Diurnal studies were carried out in 7 African-American and 7 white normal premenopausal women matched for age, weight and height to further characterize these racial differences in calcium homeostasis. Serum 25(OH)D was significantly lower and serum intact parathyroid hormone (PTH) was significantly higher in the African-American compared with the white women, whereas serum total calcium, Ca²⁺, phosphorus and 1,25-dihydroxyvitamin D [1,25(OH)₂D] were not different in the two groups. Serum intact PTH increased significantly at night in the white women and did not change in the African-American women. Urinary calcium was 47% lower in the African-American than in the white women during the day but was not different at night. Urinary calcium declined at night by 53% in the white women and by 40% in the African-American women. Stepwise multivariate analysis showed that determinants of urinary calcium were mean 24 h serum intact PTH and serum Ca²⁺ in the two groups together, mean 24 h serum intact PTH, body mass index (BMI) and serum 25(OH)D in the white women, and BMI in the African-American women. Urinary N-telopeptide of type I collagen, a marker of bone resorption, increased by over 60% at night in both groups and was 25% lower in African-American compared with white women, but the difference was not statistically different. Urinary free deoxypyridinoline also increased at night in both groups and was not racially different. Thus, African-American women show higher serum intact PTH and greater conservation of calcium than white women throughout the day. In both groups, maintenance of serum calcium at night is achieved by increased bone resorption and renal conservation of calcium. Received: 15 April 1999 / Accepted: 6 July 1999     

认知行为护理结合低磷饮食对慢性肾衰竭血液透析患者心理、营养等的影响

目的分析认知行为护理结合低磷饮食对慢性肾衰竭血液透析患者心理、营养等影响。方法将我院2019年1月至2021年1月64例慢性肾衰竭血液透析者按随机数字表法分为对照组(常规护理)和观察组(认知行为护理结合低磷饮食),评估SDS和SAS评分、依从性、营养指标(血磷、前白蛋白、白蛋白)、护理满意率。结果护理后观察组SAS、SDS分值低于对照组,饮食、用药、液体摄入、透析依从评分高于对照组,血磷低于对照组,前白蛋白、白蛋白高于对照组,护理满意率(96.88%)高于对照组(75.00%),以上比较均有统计学意义(P<0.05)。结论认知行为护理结合低磷饮食能提高慢性肾衰竭血液透析患者治疗和护理依从性,改善机体营养状态和心理状态,提高护理满意度。     

人甲状旁腺组织体外培养及高磷的影响

RT—PCR检测人甲状旁腺有无磷钠转运体Pit-1mRNA表达；高磷、膦甲酸钠（PFA）刺激体外培养的人甲状旁腺组织，观察PTH分泌量的变化。发现甲状旁腺表达Pit-1；高磷通过作用于Pit-1促进PTH分泌，而PFA抑制其分泌。     

Inherited hypophosphatemic disorders in children and the evolving mechanisms of phosphate regulation

Phosphorous is essential for multiple cellular functions and constitutes an important mineral in bone. Hypophosphatemia in children leads to rickets resulting in abnormal growth and often skeletal deformities. Among various causes of low serum phosphorous are inherited disorders associated with increased urinary excretion of phosphate, including autosomal dominant hypophosphatemic rickets (ADHR), X-linked hypophosphatemia (XLH), autosomal recessive hypophosphatemia (ARHP), and hereditary hypophosphatemic rickets with hypercalciuria (HHRH). Recent genetic analyses and subsequent biochemical and animal studies have revealed several novel molecules that appear to play key roles in the regulation of renal phosphate handling. These include a protein with abundant expression in bone, fibroblast growth factor 23 (FGF23), which has proven to be a circulating hormone that inhibits tubular reabsorption of phosphate in the kidney. Two other bone-specific proteins, PHEX and dentin matrix protein 1 (DMP1), appear to be necessary for limiting the expression of fibroblast growth factor 23, thereby allowing sufficient renal conservation of phosphate. This review focuses on the clinical, biochemical, and genetic features of inherited hypophosphatemic disorders, and presents the current understanding of hormonal and molecular mechanisms that govern phosphorous homeostasis.     

Phosphorus magnetic resonance spectroscopy studies in schizophrenia

Phosphorus magnetic resonance spectroscopy (³¹P MRS) allows in vivo quantification of phosphorus metabolites that are considered to be related to membrane turnover and energy metabolism. In schizophrenia (SZ), ³¹P MRS studies found several abnormalities in different brain regions suggesting that alterations in these pathways may be contributing to the pathophysiology. In this paper, we systematically reviewed the ³¹P MRS studies in SZ published to date by taking patient characteristics, medication status and brain regions into account. Publications written in English were searched on http://www.ncbi.nlm.nih.gov/pubmed/, by using the keywords ‘phosphomonoester’, ‘phosphodiester’, ‘ATP’, ‘phosphocreatine’, ‘phosphocholine’, ‘phosphoethanolamine’,‘glycerophosphocholine’, ‘glycerophosphoethanolamine’, ‘pH’, ‘schizophrenia’, and ‘MRS’. Studies that measured ³¹P metabolites in SZ patients were included. This search identified 52 studies. Reduced PME and elevated PDE reported in earlier studies were not replicated in several subsequent studies. One relatively consistent pattern was a decrease in PDE in chronic patients in the subcortical structures. There were no consistent patterns for the comparison of energy related phosphorus metabolites between patients and controls. Also, no consistent pattern emerged in studies seeking relationship between ³¹P metabolites and antipsychotic use and other clinical variables. Despite emerging patterns, methodological heterogeneities and shortcomings in this literature likely obscure consistent patterns among studies. We conclude with recommendations to improve study designs and ³¹P MRS methods in future studies. We also stress the significance of probing into the dynamic changes in energy metabolism, as this approach reveals abnormalities that are not visible to steady-state measurements.     

Contribución de fósforo y PTH al desarrollo de hipertrofia y fibrosis cardíaca en un modelo experimental de insuficiencia renal crónica

Background and objectiveAdequate serum phosphorus levels in patients with chronic kidney disease is essential for their clinical management. However, the control of hyperphosphatemia is difficult because is normally associated with increases in serum PTH. In the present study, the effects of hyperphosphatemia, in the presence of elevated and normal PTH, on cardiac inflammation, hypertrophy and fibrosis in an experimental renal failure model were analyzed.Materials and methodsFour groups of rats were formed. Two groups underwent total parathyroidectomy (PTx). Rats with Ca < 7.5 mg/dL and PTH < 50 pg/mL underwent 7/8 nephrectomy (CRF) and a subcutaneous pellet was placed that releases PTH 1-34 (5 μg/kg/day). One group received a diet with normal P (NP) (CRF + PTx + rPTH + NP group) and another with a high P diet (0.9% HP) (CRF + PTx + rPTH + HP group). Other two groups that only had CRF received NP (CRF + NP) and HP (CRF + HP) diet. A SHAM group for nephrectomy and parathyroidectomy was also added. After 14 weeks the rats were sacrificed.ResultsThe groups with a diet high in phosphorus (CRF + H A and CRF + PTx + rPTH + HP) had a significant reduction in creatinine clearance and also in body weight with an increase in serum phosphorus regardless of parathyroidectomy, but not serum levels of calcium, FGF23 and calcitriol that were 2-3 times higher in the group with secondary hyperparathyroidism (CRF + HP).The diameter of the cardiomyocytes was greater in the CRF + HP group, while parathyroidectomy (CRF + PTx + rPTH + HP) significantly reduced them, despite the high and similar serum phosphorus values. TNF-α, Adam17 and cardiac fibrosis at the histological and molecular level showed a similar pattern with increases in the group with severe secondary hyperparathyroidism (CRF + HP).ConclusionsHyperphosphatemia confirmed its importance in the genesis of secondary hyperparathyroidism, but also of kidney damage that was independent of PTH levels. However, inflammation, fibrosis, and cardiomyocyte growth were more closely related to PTH levels, since in the presence of similar severe hyperphosphatemia, parathyroidectomy reduced the values of inflammatory parameters, cardiac hypertrophy, and fibrosis.     

慢性肾脏病患者成纤维细胞生长因子23与肾功能及钙磷代谢的关系

目的 探讨慢性肾脏病（CKD）患者随着肾功能的变化,其成纤维细胞生长因子23（FGF23）与钙磷代谢的关系。 方法 研究对象为2008年8月至2009年4月在上海交通大学附属第一人民医院肾内科住院的初诊CKD患者72例,按照肾小球滤过率（GFR）水平分为5组,另设健康对照组20例。抽取受试者静脉血并分离血清,以酶联免疫法检测FGF23、25（OH）VitD3、1,25（OH）2VitD3;全自动生化分析仪测量钙（Ca）、磷（P）、血肌酐（Scr）、尿素氮（BUN）、白蛋白（Alb）水平;免疫放射法测定全段甲状旁腺激素（iPTH）。 结果 CKD患者血清FGF23水平随GFR降低逐渐升高,在CKD4期和5期时,血FGF23、P、iPTH上升明显,1,25（OH）2VitD3显著下降,与CKD1期差异有统计学意义（均P < 0.05）。CKD2~3期与CKD1期的FGF23、P、Ca、iPTH、活性维生素D水平差异均无统计学意义。血Ca、25（OH）VitD3随着肾功能下降有降低趋势,但各期间差异均无统计学意义。Pearson相关分析显示,CKD1~5期logFGF23与P、logiPTH呈正相关（r = 0.653,P < 0.01;r = 0.800,P < 0.01）,与GFR、1,25（OH）2VitD3呈负相关（r = -0.753,P < 0.01;r = -0.265,P < 0.05),与Ca、25（OH）VitD3无相关。CKD1~3期logFGF23与logiPTH呈正相关(r = 0.374,P < 0.05),而与Ca、P、25（OH）VitD3、1,25（OH）2VitD3、GFR均无相关。CKD4~5期log FGF23与P、logiPTH呈正相关（r = 0.381,P < 0.05;r = 0.515,P < 0.01）,与GFR呈负相关（r = -0.654,P < 0.01）,与Ca、25（OH）VitD3、1,25（OH）2VitD3无相关。 结论 随着肾功能减退,血清FGF23、P、iPTH水平逐渐升高,活性维生素D水平逐渐下降,尤以CKD4~5期明显。在肾脏病早期阶段（CKD1~3期）血iPTH水平与FGF23有关。当GFR<30 ml/min时,肾功能状态、血磷、血iPTH均可影响血FGF23水平。