血液及腹膜透析对肾性骨病患者血清生化指标的影响

目的探讨血液透析（HD）及腹膜透析（PD）对终末期肾病患者骨代谢血清生化指标的影响。方法将患者按所采用的透析方式随机分为HD组及PD组,分别检测两组患者血清骨碱性磷酸酶（BALP）、抗酒石酸酸性磷酸酶（TRAP5b）、钙、磷、全段甲状旁腺激素（iPTH）及骨密度。结果 HD组及PD组之间钙、磷及iPTH、BALP差异均无统计学意义;与PD组比较,HD组血清TRAP5b水平高,在腰椎部位的骨密度低（P〈0.05）。结论 PD治疗对于肾性骨病血清破骨细胞活性的指标及腰椎骨密度控制情况优于HD治疗。     

维持性血液透析患者慢性肾脏病-矿物质及骨代谢异常

目的调查吉林省人民医院维持性血液透析(MHD)患者患慢性肾脏病-矿物质及骨代谢异常(CKD-MBD)的基本情况,比较分析老年组及非老年组的差别,并进一步探讨影响全段甲状旁腺激素(iPTH)升高的相关因素。方法选取该中心MHD患者168例为研究对象,按照年龄分为老年组(n=86)和非老年组(n=82),收集患者一般资料,iPTH、血磷、血钙、碱性磷酸酶、血红蛋白、血清白蛋白、血糖、尿素氮等指标,根据2017年KDIGO发表的最新指南比较两组各指标的达标率及特点,并对导致iPTH升高的相关因素进行单因素及多因素回归分析。结果该中心MHD患者中低转运型骨病的患病率为16.07%,高转运型骨病的患病率为26.19%,老年组中低转运型骨病的患病率为18.60%,高转运型骨病的患病率为17.44%,非老年组中低转运型骨病的患病率为13.41%,高转运型骨病的患病率为35.37%。两组间比较非老年组iPTH、血磷及尿素氮均不同程度显著高于老年组(P0.05)。老年组iPTH、血钙的达标率均低于非老年组,而老年组血磷达标率(51.16%)显著高于非老年组(19.51%,P0.05)。对导致iPTH升高的相关因素进行Logistic回归分析显示:年龄的降低及透析龄增加为iPTH升高的独立危险因素。结论 MHD患者中,老年患者易患低转运型骨病,年轻患者易患继发性甲状旁腺功能亢进,而透析龄亦可能是诱发继发性甲状旁腺功能亢进的危险因素。     

CKD-MBD的诊断是否必须依赖骨活检

<正>慢性肾脏病(CKD)已成为全球性公共卫生问题,其发病率日益升高,且预后较差。矿物质代谢异常在CKD 2期即已出现,患者如未得到及时诊治,终将发生代谢性骨病(肾性骨营养不良)。2005年,KDICO将肾性骨营养不良重新定义并扩大诊断为慢性肾脏病矿物质和骨异常(CKD-MBD),包括以下三种异常:(1)钙、磷、甲状旁腺激素和维生素D代谢异常;(2)骨转运、骨矿化、骨容量和骨的生长异常;(3)血管和软组织钙化。其中,肾性骨营养不良特指CKD-MBD中经四环素标记骨活检确诊的一类疾病。由于骨活检属于侵     

成年血液透析患者矿物质及骨代谢紊乱调查

目的 调查江苏省昆山市第一人民医院维持性血液透析（maintenance hemodialysis,MHD）患者的慢性肾脏病矿物质及骨代谢异常（chronic kidney disease-mineral and bone disorders,CKD-MBD）情况,比较分析老年和非老年患者CKD-MBD的特点,为临床治疗提供依据.方法 调查234例MHD患者的透析龄、透前肌酐、血小板、白蛋白、血色素、血钙、血磷、ALP及iPTH的水平及临床资料,与指南比较分析老年组和非老年组血钙、血磷、ALP及iPTH的特点.结果 我院MHD患者非老年组患病率高于老年组（P＜0.05）;透析龄、干体重、透前肌酐、白蛋白水平等指标两组间差异无统计学意义（P＞0.05）;血清钙、磷、iPTH达标率分别为83.76％、19.66％、40.17％.两组比较,老年组血清钙、磷、iPTH、ALP均不同程度的低于非老年组,差异有统计学意义（P＜0.05）.结论 老年组MHD患者CKD-MBD指标低于非老年组,提示两组患者CKD-MBD发生机制存在差异,老年患者容易合并低转运骨病（akinesis bone disease,ABD）.     

低转化性肾性骨病的诊断研究进展

肾性骨病,又称为肾性骨营养不良,即慢性肾病—矿物质和骨代谢紊乱,其发生率在维持性血液透析患者几乎达100%。目前,临床上主要根据血清全段甲状旁腺激素(iPTH)浓度将肾性骨病分为3种:高转化型肾性骨病、低转化型肾性骨病和混合型肾性骨病,低转化性肾性骨病又可分为骨软化症和     

慢性肝病患者骨营养不良的临床分析

慢性肝病时可引起全身多系统的损害，尤其是血清钙和磷的吸收障碍，维生素D和钙、磷的代谢失衡，骨密度减低，引起肝性骨营养不良。本文就慢性肝病患者血清钙、磷与甲状旁腺素、降钙素及骨密度的变化，分析肝性骨病的发生机制。     

腺嘌呤诱导肾性骨病大鼠模型的生物力学分析

目的:观察腺嘌呤诱导的慢性肾脏病(CKD)肾性骨病大鼠模型的腰椎及股骨的生物力学特点。方法:20只雄性SD大鼠分为正常对照组和CKD组。第6周末处死大鼠,行血清生化标志物检测,取股骨和第五腰椎做骨密度(BMD)及骨生物力学分析。结果:在第6周末,CKD组大鼠血清尿素氮、血清肌酐、血清无机磷、血清甲状旁腺激素较正常对照组均明显升高,血清钙明显降低。与正常对照组比较,CKD组的股骨和第五腰椎椎体BMD均明显降低。骨生物力学,股骨三点弯曲实验结果提示,CKD组大鼠的股骨结构力学指标和材料力学指标均明显降低;腰椎压缩实验结果提示,CKD组大鼠腰椎的结构力学指标和材料力学指标均明显降低。结论:腺嘌呤诱导的大鼠CKD模型能较好地模拟CKD时出现的高转运肾性骨病的生物力学特征,表现为皮质骨和松质骨材料力学和结构力学性能的下降,有望成为CKD肾性骨病模型的研究载体。     

慢性肾衰患者的罗钙全应用

罗钙全作为la，25－H羟基维生素D制剂用于临床已有近20年的历史，对预防和治疗肾性骨病起了重要的作用’‘’。但是，随着对肾性骨病研究的不断深入，尤其是骨活检术及全段甲状旁腺素（intactParathyylodh00－mone，iPTH）测定的普遍开展，人们对肾性骨病的认识较以前发生了很大的变化。这些改变也对罗钙全的应用产生了一定的影响。本文就罗钙全治疗肾性骨病的临床研究进展作一综述。1肾性骨病的病理生理特点继发性甲状分腺功能亢进几乎是所有慢性肾衰患者的常见合并症，无论是已经采取透析治疗还是在非透析阶段的患者，常常表现为纤维囊…     

维持性血液透析患者骨组织形态学变化与血生化指标的相关性研究

目的 :了解肾性骨营养不良在血液透析患者中的发病及分布情况 ,观察血生化指标与骨组织形态学有关参数的相关性。　 方法 :对 15例血液透析患者行骨活检 ,进行骨活检标本骨组织形态计量学检测 ,同时测定某些血生化指标。　 结果 :15例血液透析患者均有程度不等、变化不一的骨组织学病理变化 ;全段甲状旁腺激素(intactparathyroidhormone ,iPTH)与骨矿化率、骨形成率具有相关性 (r=0 5 85 ,P <0 0 5 ;r =0 436 ,P <0 0 5 )。骨特异性碱性磷酸酶 (bonealkalinephosphatase ,BAP)、碱性磷酸酶 (alkalinephosphatase ,ALP)均与类骨质表面、类骨质面积呈正相关关系 ,前者相关性更好 (r=0 70 1vs 0 5 32 ;r=0 82 7vs 0 80 9)。血iPTH在低转化骨病与非低转化骨病两组间差异显著 (P <0 0 1)。 2例铝中毒骨病患者 ,血清铝在正常范围内 ,去铁胺试验后血铝增加值较非铝中毒者高 ,而且iPTH水平较低。　 结论 :iPTH、BAP结合起来可以初步估计骨代谢状态 ;而在铝中毒骨病的诊断上 ,去铁胺试验结合血iPTH水平有一定帮助。但以上血生化指标在不同类型的骨病中并无严格的界限 ,所以 ,骨活检仍是诊断肾性骨营养不良的金标准。     

慢性肾脏病矿物质和骨异常患者骨折风险评估及临床意义

人类认识到慢性肾脏病(chronic kidney disease,CKD)与骨的密切关系最早可以追溯到1942年,北京协和医院的刘世豪在Science首次命名了因为肾脏病导致的骨病,即"肾性骨营养不良"(renal osteodystrophy,简称肾性骨病),并提出双氢速变固醇治疗有效[1]。随后大量的证据表明CKD可导致钙、磷、碱性磷酸酶(alkaline phosphatase, ALP)、甲状旁腺     

Diffuse soft tissue and vascular calcification in systemic lupus erythematosus with chronic kidney disease

The systemic disorder of mineral and bone metabolism which is related to chronic kidney disease (CKD) is called mineral and bone disorder (MBD). Calcifications related to CKD-MBD may occur in ophthalmic tissue, arterial walls, subcutaneous and periarticular soft tissues and organs. The vascular calcifications are the most important causes of mortality and morbidity in CKD. Here, we present a case of systemic lupus erythematosus with early and disseminated calcifications of vascular and periarticular soft tissues related to CKD-MBD.     

Troubles minéraux et osseux dans la maladie rénale chronique : physiopathologie,conséquences et prise en charge

Chronic Kidney Disease (CKD) is associated with a strong impact on phosphocalcic homeostasis, due to the chronic reduction in glomerular filtration rate (GFR) (phosphate excretion decrease), the inhibition of calcitriol synthesis and dietary restrictions. CKD-Mineral and Bone Disorders (CKD-MBD) must be monitored in CKD patients with biological work-up associated with bone markers and bone density dual X-ray absorptiometry. Adapted diet (phosphate restriction, normalization of calcium intake) and medications (vitamin D, phosphate binders, calcimimetics) help to correct CKD-MBD. Serum parathormone must be kept between 2 to 9 times the usual values, to limit renal osteodystrophy and avoid tertiary hyperparathyroidism. CKD patients are also at risk of artery calcifications, which can significantly increase the morbidity and mortality of the affection. Bisphosphonates may be used after correction of biological abnormalities, in patients with estimated GFR above 30 ml/min/1,73 m². Even if transplantation aims to normalize kidney function, kidney transplant recipients remain at risk of CKD-MBD. Biology and bone density dual X-ray absorptiometry must be regularly assessed, especially in the few months following the transplantation. More studies are needed to know if treatments of CKD-MBD are well tolerated in severe CKD and if they are associated with a decrease of bone fracture and vascular calcifications.     

Chronic Kidney Disease-Mineral Bone Disorder: Definitions and Rationale for a Systemic Disorder

Over the past decade there has been an increasing awareness of the complexity of bone and mineral complications observed in chronic kidney disease (CKD) and recognition that the consequences of these abnormalities affect not only the skeleton, but also the cardiovascular system. These scientific advances led to the naming of a systemic disorder, ??Chronic Kidney Disease-Mineral Bone Disorder?? (CKD-MBD) defined as abnormalities in mineral-related biochemistries, bone modeling/remodeling and strength, and extraskeletal calcification. CKD-MBD begins early in the course of progressive CKD, at estimated glomerular filtration rates of 60?ml/min or earlier, with progression such that all dialysis patients have one or more components. The older term, renal osteodystrophy is one component of CKD-MBD and should be used exclusively to define the histopathologic abnormalities of CKD-related bone remodeling. This diagnostic criteria has been further refined using a new classification system ??turnover, mineralization, and volume??, that defines bone turnover, mineralization, and volume to allow for a more complete evaluation of renal osteodystrophy. The recognition of this inter-relationship between biochemical changes, bone, and extraskeletal calcification as the systemic disorder CKD-MBD allows for enhanced communication, increased awareness/diagnosis, and improved treatment approaches with the ultimate goal of improving morbidity and mortality in patients with CKD.     

Adynamic bone disease: Revisited

The bone and mineral disorders form an integral part of the management of a chronic kidney disease (CKD) patient. Amongst various types of bone pathologies in chronic kidney disease-mineral bone disorder (CKD-MBD), the prevalence of adynamic bone disease (ABD) is increasing. The present review discusses the updated pathophysiology, risk factors, and management of this disorder.     

CKD-MBD beim betagten Patienten

Chronic kidney disease (CKD) is frequently associated with disturbed mineral and bone metabolism and greatly contributes to morbidity and mortality. Concerning the choice of renal replacement therapy, the elderly have been regarded differently than the younger CKD population. However, there is a major lack of data regarding the management of CKD mineral and bone disorders (CKD-MBD). Current KDIGO guidelines do not emphasize specific diagnostics and therapy of CKD-MBD in the elderly. The elderly patient should thus be approached individually with consideration to age, comorbidities and quality of life in order to cope with the special needs of aged patients with CKD-MBD. In very elderly patients with higher morbidity and reduced life expectancy the very strict recommendations concerning diagnostics and therapy can probably be relaxed.     

Treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD)

Disturbances in mineral and bone metabolism play a critical role in the pathogenesis of cardiovascular complications in patients with chronic kidney disease (CKD). The term "renal osteodystrophy" has recently been replaced with "CKD-mineral and bone disorder (CKD-MBD)", which includes vascular calcification as well as bone abnormalities. Following this paradigm shift, the Japanese Society for Dialysis Therapy released guidelines for the management of secondary hyperparathyroidism in chronic dialysis patients, which prioritized improvement in survival, but not in bone abnormalities. According to these guidelines, parathyroid intervention, such as parathyroidectomy and percutaneous ethanol injection therapy, should be indicated if mineral disorders cannot be managed by pharmacological means. Recently, several novel therapeutic tools, including sevelamer hydrochloride, calcitriol analogs, and cinacalcet hydrochloride have been introduced in the clinical setting in Japan. Harmonizing these therapeutic modalities, we should expect more effective management of CKD-MBD, leading to the improvement of morbidity and mortality in this patient population.     

Biochemical Abnormalities in Chronic Kidney Disease–Mineral Bone Disease

Chronic kidney disease?Cmineral and bone disorders (CKD-MBD) is a term introduced by the Kidney Disease: Improving Global Outcomes (KDIGO) work group on mineral and bone disorder as a syndrome of interrelated biochemical, bone, and vascular abnormalities encountered in CKD. Biochemical abnormalities in CKD represent primary indicators for the diagnosis and management of CKD-MBD. This review discusses each abnormality separately, with references to both the Kidney Dialysis Outcomes Quality Initiative (KDOQI) Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease and KDIGO Guidelines for Mineral and Bone Disorder. Selected references to the association between biochemical abnormalities and adverse clinical outcomes in CKD population are provided.     

Clinical Features and Manifestations of CKD-MBD

Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a complex interplay of risk factors, diseases and outcomes. In the last two decades, there has been a steady drift towards definitions depending ever more closely on laboratory abnormalities, which only represent at best possible risk factors for downstream pathology. In the early years of nephrology, especially when the therapeutic agents we had available to combat CKD?CMBD were modest, bone and muscle problems were often advanced, and symptomatic, with bone and muscle pain, fractures and myopathy. This ??old style?? hyperparathyroidism paradigm has become substantially less common now, and we can forget how symptomatic, and how draining of life-quality, CKD-MBD can be. In this chapter, we explore in the main the most feared complication of all, that of a fracture, which not only are dramatically more common in CKD patients, but also have a much heightened mortality over similar fractures but not in a CKD setting.     

Pediatric Patients with Chronic Kidney Disease-Mineral Bone Disorder

Chronic kidney disease-mineral bone disorder (CKD-MBD) is a systemic disorder of mineral and bone metabolism that has deleterious consequences on skeletal and cardiovascular health. Nowhere is the morbidity of this disorder more telling than in children. During childhood and adolescence, CKD-MBD may result in poor growth and skeletal deformities, while the mineral dysregulation can manifest in cardiovascular disease in early adulthood, a development that places the patients at high risk for severe morbidity and early mortality. Unfortunately, management of CKD-MBD has been less than satisfactory in children despite recent advances and is limited by the lack of evidence-based treatment guidelines. More positive are ongoing research efforts, such as the Chronic Kidney Disease in Children and the Cardiovascular Comorbidity in Children with CKD (4C) studies that are currently providing important insights which should help better elucidate the pathogenesis and progression of mineral dysregulation and its clinical impact in children. Data from these studies and others will undoubtedly also help formulate clinical trials and the generation of evidence-based therapeutic options designed to provide more effective management of CKD-MBD in the pediatric population.     

Guideline-practice gap in the management of predialysis chronic kidney disease mineral bone disorder in Japan

No study has reported the current status of the management of chronic kidney disease mineral bone disorder (CKD-MBD) in Japan. Using the Osaka Vitamin D Study in CKD (OVIDS-CKD), we examined the prevalence of patients with serum calcium, phosphate, parathyroid hormone (PTH), or 25-hydroxyvitamin D levels outside the target of KDOQI guidelines. Eighty-four percent of the patients had 25-hydroxyvitamin D <30 ng/mL. Significant determinants of poor vitamin D status were female gender, diabetes, high PTH, and high urinary protein (2+ or greater). The percentage of patients with intact PTH higher than the target was 8% in CKD stage 3a, while between 20-22% in stages 3b to 5. The patients indicated for ergocalciferol were 7, 18, and 19% in stages 3a, 3b, and 4, respectively, and those indicated for active vitamin D were 21% in stage 5. Since neither ergocalciferol nor cholecalciferol is available in 2011 in Japan, we have no choice but to prescribe alfacalcidol or calcitriol; however, the percent of patients receiving these drugs was only 1, 4, 8, and 14% in stages 3a, 3b, 4, and 5, respectively, indicating that PTH and vitamin D status are not well controlled in Japan. In contrast, more than 80% of the patients met the target of serum calcium and phosphate. Contrary to expectations, nearly 20% of the patients had hypophosphatemia in stage 3 and 5, possibly because of strict protein restriction. Given these results, nephrologists should consider prescribing active vitamin D, especially for females and patients with diabetes, massive proteinuria, or secondary hyperparathyroidism.