不同钙浓度腹膜透析液对长期CAPD患者矿物质和骨代谢影响的分析

目的观察腹膜透析液钙离子浓度对持续性不卧床腹膜透析(CAPD)患者矿物质和骨代谢的影响。 方法回顾性分析我院腹膜透析中心行CAPD治疗2年以上的123例患者,根据腹膜透析液钙离子浓度分为低钙腹膜透析液组(LCD组,钙离子浓度为1.25 mmol/L)和标准钙腹膜透析液组(SCD组,钙离子浓度为1.75 mmol/L),观察不同钙浓度腹膜透析液对患者血清钙、磷、全段甲状旁腺激素(iPTH)、颈动脉厚度、心脏瓣膜钙化及骨痛、皮肤瘙痒等情况的影响。使用SPSS 18.0统计软件包进行数据处理。 结果2组患者治疗前人口学特征、腹膜转运特性、钙磷代谢等指标的基线水平差异无统计学意义(P>0.05)。治疗2年后,2组患者血钙浓度及达标率较治疗前均显著增高(P<0.05),SCD组血钙浓度增幅高于LCD组,但差异无统计学意义(0.26±0.31 mmol/L与0.17±0.29 mmol/L, t＝1.621,P＝0.108);2组间治疗后血清钙、磷、iPTH平均水平及其达标率、颈动脉厚度、心脏瓣膜钙化比例、骨痛及皮肤瘙痒累计发生率差异均无统计学意义(P>0.05);LCD组活性维生素D使用比例显著高于SCD组(χ² ＝6.373,P<0.05)。 结论采用低钙与标准钙腹透液治疗2年,对CAPD患者矿物质和骨代谢的影响无显著性差异。     

Relationship between glucose exposure via peritoneal dialysis solutions and coronary artery calcification in non-diabetic peritoneal dialysis patients

Introduction

Vascular calcification is frequent in dialysis patients and is associated with increased mortality. Impaired glucose metabolism is proposed as a contributing factor for vascular calcification. We investigated whether glucose exposure via dialysate may have a role in vascular calcification in non-diabetic peritoneal dialysis patients.

Method

We measured coronary artery calcification by multi-slice computerized tomography in 50 prevalent non-diabetic peritoneal dialysis patients and assessed its relations with fasting blood glucose, homeostasis model assessment of insulin resistance (HOMA-IR), and glucose exposure from peritoneal dialysis fluid.

Results

Twenty-four patients (48%) had no coronary calcification. When patients were grouped according to the presence or absence of calcification, patients with calcification were mostly men and had higher burden of cardiovascular disease history, vitamin D dose intake, serum calcium, total glucose exposure from dialysis solution, and lower total weekly Kt/V _urea. In multivariate analysis, dialysate glucose exposure was an independent predictor of coronary artery calcification score, besides serum calcium and Kt/V _urea.

Conclusion

These data suggest that high glucose exposure from dialysis solution, which is potentially correctable, is a risk factor for vascular calcification in non-diabetic PD patients.     

We Use Dialysate Potassium Levels That Are Too Low in Hemodialysis

Sudden cardiac death accounts for a quarter of all deaths in hemodialysis patients. While this group is at high risk for cardiovascular events, there are certain modifiable factors that have been associated with higher risk of sudden cardiac death. These include short dialysis time, high ultrafiltration rate, and dialysate with a low potassium or calcium concentration. While it is impossible to discern the relative contribution of each of these factors, our review focuses on the role of dialysate potassium concentration in sudden cardiac death. Retrospective studies have identified low potassium dialysate (<2–3 mEq/l) as a risk factor for sudden cardiac death, particularly in patients with predialysis serum potassium concentrations <5 mEq/l. However, patients with predialysis hyperkalemia (≥5.5 mEq/l) may be an exception since a significant association of low potassium dialysate with sudden cardiac death was not observed in this subgroup. Dialysis prescribers must employ alternatives to low dialysate potassium concentrations to achieve potassium control such as increasing dialysis time and frequency, dietary restriction of potassium, prevention and treatment of constipation, discontinuation of medications contributing to hyperkalemia and traditional (or newer, better tolerated) potassium binding resins. Finally, one must also address other factors associated with sudden cardiac death such as short dialysis time, high ultrafiltration rate, and low calcium concentration dialysate.     

Calcium exposure and removal in chronic hemodialysis patients.

The risks associated with calcium exposure in chronic hemodialysis (HD) patients are becoming increasingly apparent. Current K/DOQI guidelines recommend an absolute maximum elemental calcium load of 2,000 mg/d, including calcium-containing medication and a maximum dialysate calcium concentration of 1.25 mmol/L (to avoid intradialytic calcium loading). The goal of this study was to characterize the total exposure to calcium from all sources that chronic HD patients are exposed to. We studied 52 patients. Each was requested to complete a 3-day food diary for analysis of daily calcium intake; 24-hour urine collections were taken and analyzed for calcium content. All patients underwent HD using Hospal Integra (Lyon, France) dialysis monitors, bicarbonate buffering, and dialysate sodium and calcium concentrations of 134 mmol/L and 1.25 mmol/L, respectively. Blood was sampled before and after HD for total serum calcium, albumin, bicarbonate, and phosphate, in addition to ionized calcium level measured at the bedside using a portable electrolyte analyzer. Calcium flux was determined from measurements of ionized calcium levels in dialyzer inlet samples and those in continuous partial waste dialysis collection (with reference to total waste dialysate and ultrafiltration volumes). There was marked interpatient variability of total calcium exposure; the mean was 2,346 +/- 293 mg (range, 230 to 7,309 mg) per day. The majority of enteral calcium exposure was from calcium-containing phosphate binders, with diet providing only a mean load of 581 +/- 34 mg (range, 230 to 1,309 mg). Calcium removal was evident in 83% of patients. Mean calcium flux was -187 +/- 232 mg (range, -486 to 784 mg). There was a linear correlation observed between the amount of calcium removed during dialysis and the predialysis ionized plasma calcium concentration, r2 = 0.42, P < .001 (calculated from actual measured dialysate ionized calcium concentration). This shows that calcium flux across the dialysis membrane is determined by the diffusion gradient. The amount of calcium removed during dialysis was found to be independent of exogenous calcium load. These results support previous reported data showing that the majority of HD patients are continually experiencing calcium overload. This may have a contributory role in the development of vascular calcification. In contrast to recent K/DOQI recommendations, an upper dialysate concentration of 1.25 mmol/L may not be ideal for every patient. To minimize the effects of exogenous calcium overload, dialysate concentrations should be prescribed with reference to plasma calcium levels.     

High‐calcium dialysate: A factor associated with inflammation,malnutrition and mortality in non‐diabetic maintenance haemodialysis patients

Aim: Chronic inflammation, which is common in dialysis patients, often causes malnutrition and even protein‐energy wasting. However, the association of high‐calcium dialysate with malnutrition and/or inflammation in non‐diabetic maintenance haemodialysis patients remains unclear. This study investigated the possible adverse effects of high‐calcium dialysate and mortality in this population. Methods: A total of 717 non‐diabetic haemodialysis patients participated in this 2 year prospective study. The subjects were categorized into three subgroups based on whether dialysate calcium concentrations were high (3.5 mEq/L), standard (3.0 mEq/L) or low (2.5 mEq/L). Demographic, haematological, nutritional and inflammatory markers, biochemical and dialysis‐related data were obtained for cross‐sectional analysis. Causes of death and mortality rates were also analyzed for each subgroup. Results: Patients with high‐calcium dialysate (n = 82) had a higher incidence of malnutrition and inflammation (61.0% vs 44.1% and 43.9%, respectively) than those with standard‐ and low‐calcium dialysate (n = 528 and 107). Backward stepwise multiple regression analysis revealed that high‐calcium dialysate was negatively correlated with nutritional index, serum albumin levels, but positively associated with the inflammatory marker of serum ferritin levels. At the end of the 2 year follow up, 45 patients had died. Cox multivariate analysis demonstrated that high‐calcium dialysate was a significant associated factor (relative risk 2.765; 95% confidence interval 1.429–5.352) for 2 year all‐cause mortality in these patients. Conclusion: The analytical results indicate that high‐calcium dialysate is associated with malnutrition and inflammation as well as 2 year mortality in non‐diabetic maintenance haemodialysis patients and the findings suggest that this population, even those with optimal mineral balance, should avoid high‐calcium dialysate.     

Impact of low calcium dialysate on survival in continuous ambulatory peritoneal dialysis patients

Objective To investigate the impact of low calcium dialysate on survival in continuous ambulatory peritoneal dialysis（CAPD）patients. Methods CAPD patients at our PD center between January 1,2006 and December 31,2010 were retrospectively studied. The patients were divided into standard - calcium dialysate (SCD) group and low - calcium dialysate (LCD) group. Cox regression analysis was used to compare patient survival and determine the related risk factors Results A total of 982 eligible PD patients were included in this study, of whom 634 patients treated with standard-calcium dialysate, and 348 with low-calcium dialysate. During a median follow-up of 24.2 - month, 162(16.5% ) died, 71(43.8% ) of them due to cardiovascular and cerebrovascular diseases. The overall 1-, 3-, and 5-year patient survival rates were 90.9%, 74.2% and 58.9% in SCD group and 98.6%, 94.0% and 76.4% in LCD group. Cox regression analysis demonstrated that low calcium dialysate treatment reduced 59% risk of all-cause death, as compared with standard calcium dialysate exposure. Old age, diabetes status and lower hematoglobin were independent risk factors of all - cause death in CAPD patients. Conclusion The survival rate of CAPD patients using LCD is obviously higer than that using SCD. Old age, diabetes status and lower haematoglobin are independent risk factors of all-cause death in CAPD patients.     

Management of disturbances of calcium and phosphate metabolism in chronic renal insufficiency, with emphasis on the control of hyperphosphataemia.

BACKGROUND: Disturbances of calcium-phosphate (Ca-P) metabolism in chronic renal insufficiency (CRI) play an important role not only in bone disease (renal osteodystrophy) but also in soft tissue calcification, with an increased risk of vascular calcification, arterial stiffness, and worsening of atherosclerosis. METHODS: Discussion in order to achieve a consensus on key points relating to pathogenesis, clinical assessment, and management of renal osteodystrophy in dialysis patients. RESULTS: Secondary hyperparathyroidism develops primarily as a consequence of reduced active vitamin D production by the kidneys and phosphate retention, with the development of hyperphosphataemia, hypocalcaemia, and increased parathyroid hormone (PTH) levels. The same factors over the long term cause parathyroid gland hyperplasia and autonomous PTH production (tertiary hyperparathyroidism). As hyperphosphataemia and increased CaxP product have been associated with increased mortality in dialysis patients, hyperparathyroidism should be prevented and managed, starting in the pre-dialysis period, by calcium/vitamin D supplementation. Hyperphosphataemia is usually treated by means of intestinal phosphate binders, but different types of binders have been used. The traditional aluminium-based phosphate binders are certainly effective, but have the drawback of side effects due to aluminium absorption (osteomalacia, encephalopathy, microcytic anaemia). Calcium-containing phosphate binders (calcium carbonate or calcium acetate) have mainly been used for the last 10-15 years. However, they aggravate metastatic calcification, particularly if they are taken together with vitamin D analogues and a high calcium dialysate concentration. New calcium- and aluminium-free phosphate binders have recently been developed and may be useful, particularly in patients with metastatic calcification and/or hypercalcaemic episodes, in order to reduce the phosphate burden in the absence of an additional calcium load. New vitamin D analogues and calcimimetic drugs are also being developed for PTH suppression, with the goal to minimize or even entirely avoid hypercalcaemia and/or hyperphosphataemia. A suitable dialysate calcium concentration is important and must take into consideration the medical therapy and the calcium balance on an individual patient basis. Surgical parathyroidectomy is the ultimate means of treating hypercalcaemic hyperparathyroidism, when medical therapy has failed. CONCLUSION: Achieving an evidence-based consensus can give clinicians a useful tool for the treatment of disturbances of Ca-P metabolism in CRI: this has become an important objective in nephrological care, particularly as ageing and increased risk of atherosclerosis have become major issues in the dialysis population.     

In Vitro Dialysis of Cytokine‐Rich Plasma With High and Medium Cut‐Off Membranes Reduces Its Procalcific Activity

Recently developed high‐flux (HF) dialysis membranes with extended permeability provide better clearance of middle‐sized molecules such as interleukins (ILs). Whether this modulation of inflammation influences the procalcific effects of septic plasma on vascular smooth muscle cells (VSMCs) is not known. To assess the effects of high cut‐off (HCO) and medium cut‐off (MCO) membranes on microinflammation and in vitro vascular calcification we developed a miniature dialysis model. Plasma samples from lipopolysaccharide‐spiked blood were dialyzed with HF, HCO, and MCO membranes in an in vitro miniature dialysis model. Afterwards, IL‐6 concentrations were determined in dialysate and plasma. Calcifying VSMCs were incubated with dialyzed plasma samples and vascular calcification was assessed. Osteopontin (OPN) and matrix Gla protein (MGP) were measured in VSMC supernatants. IL‐6 plasma concentrations were markedly lower with HCO and MCO dialysis. VSMC calcification was significantly lower after incubation with MCO‐ and HCO‐serum compared to HF plasma. MGP and OPN levels in supernatants were significantly lower in the MCO but not in the HCO group compared to HF. In vitro dialysis of cytokine‐enriched plasma samples with MCO and HCO membranes reduces IL‐6 levels. The induction of vascular calcification by cytokine‐enriched plasma is reduced after HCO and MCO dialysis.     

Association of dialysate calcium concentration with fetuin a level and carotid intima-media thickness in peritoneal dialysis patients

Serum fetuin A has been shown to be associated with the risk of vascular calcification and atherosclerosis, and it can predict the onset of cardiovascular mortality in dialysis patients. The carotid intima-media thickness (cIMT) is an accessible and reliable method to identify the subclinical atherosclerosis. The aim of this study was to investigate the relationships between dialysate calcium concentrations and fetuin A or cIMT in patients undergoing peritoneal dialysis (PD). Forty patients, newly diagnosed end-stage renal disease (ESRD) and undergoing peritoneal dialysis, were enrolled in the study, with a calcium content of the peritoneal dialysis (PD) solution of 1.25?mmol/L in 20 patients (low-Ca group) and 1.75?mmol/L in 20 patients (standard-Ca group). The patients were followed up for 12 months after the PD conducted. Serum fetuin A was determined using a human fetuin A enzyme-linked immunosorbent assay kit and cIMT was detected using ultrasonic wave. We observed no difference between two groups with regard to the baseline data of fetuin A, cIMT, calcium, phosphorus, calcium-phosphorus product, high sensitivity CRP (hsCRP), parathyroid hormone (PTH), or lipid parameters. After 12 months follow-up, fetuin A (263.92?±?16.1 vs. 282.76?±?21.0, p?=?0.017) and calcium-phosphorus product (39.85?±?7.76 vs. 47.50?±?6.65, p?=?0.009) were obviously lower in the low-Ca group than standard-Ca group, the other serum parameters were not different between these two groups. Compared with baseline data, serum fetuin A concentration significantly reduced in low-Ca group (?p?p?相似文献   

Management of the Dialysis Patient with Sickle Cell Disease

While patients with sickle cell disease currently constitute a very small minority of the US dialysis population (0.1%), there is anticipated growth of this group as the life expectancy of those with sickle cell disease (SCD) increases. SCD patients suffer a high burden of morbidity, which is enhanced by the presence of end‐stage renal disease (ESRD). In this review, we discuss the pathophysiology of SCD and the basic tenets of its management with focus on the dialysis patient with SCD. Anemia in dialysis patients with SCD is a unique challenge. The hemoglobin target in SCD dialysis patients with ESRD should not exceed 10 g/dl. SCD patients, and particularly those on dialysis, are likely to be poorly responsive to erythropoietin‐stimulating agent (ESA) therapy and might be at increased risk for vaso‐occlusive crisis (VOC) with ESA. Iron chelation and hydroyxurea therapy require special considerations and modifications in dialysis patients with SCD. There are theoretical advantages to both hemodialysis (HD) and peritoneal dialysis (PD) in SCD patients. With HD, there is a secure vascular access available for both standard and exchange blood transfusion in patients who need them. With PD, the absence of an acute rise in hematocrit with ultrafiltration (UF) might offer lower risk of VOC. During VOC, reduction in UF goals should be considered but administration of intravenous fluids should be reserved only for clear cases of volume depletion. Finally, renal transplantation appears to confer a survival advantage to dialysis in SCD patients and should be pursued when possible.     

Vascular calcification in South African dialysis patients: Ethnic variation, prevalence, detection and haemodynamic correlates

Aim: Studies from the US have shown little effect of ethnicity on vascular calcification in dialysis patients. This has not been examined in the multi‐ethnic population of South Africa where genetic and environmental differences may exist. We assessed the extent and severity of vascular calcification in South African dialysis patients according to race and known risk factors. We further evaluated the association of abdominal aorta calcification with coronary artery calcification. Method: Seventy‐five CKD‐5D patients and 20 healthy controls were enrolled consecutively. All subjects underwent chest computed tomography for coronary calcium score and abdominal X‐ray for abdominal aorta calcium score. Ambulatory blood pressure monitoring was generated via radial artery applanation tonometry. Results: Coronary calcification was present in 38.6% of patients and was associated with age and prior cardiovascular disease on multivariate analyses. The median coronary calcium score in black patients was 0 (IQR 0) and 66 in non‐Blacks (IQR 383, P < 0.001); controls had a coronary calcium score of 0 (IQR 0). Black race remained a significant negative predictor for coronary calcification after adjustment, prevalence ratio = 0.14 and 95% confidence interval (CI): 0.0–0.53. Vascular calcification was not associated with any ambulatory blood pressure parameter. Using receiver operator characteristic curves, an abdominal aorta calcification score of ≥1 showed an area under the curve of 0.83 to predict a coronary calcium score ≥ 10. Conclusion: Black race appears to protect from vascular calcification in South African CKD‐5D patients and this warrants further study regarding the underlying mechanism. The abdominal X‐ray is a useful screening tool for coronary calcification.     

生理浓度钙透析液对伴低甲状旁腺素水平血液透析患者矿物质及骨代谢的影响

目的观察生理浓度钙透析液对伴低甲状旁腺素水平血液透析患者矿物质及骨代谢的影响。方法将48例血清iPTH(65～150pg/ml)伴校正钙水平≥2.37mmol/L患者按使用透析液钙浓度不同随机分为:透析液钙浓度1.50mmol/L(DCa-1.50)与1.25mmol/L(DCa-1.25)两组;两组内按是否口服骨化三醇随机分为两亚组:口服骨化三醇(+Calcitriol)与非口服骨化三醇(-Calcitriol)组;治疗6个月。每3个月检测透前血清Ca,P,iPTH,ALP及BGP指标。结果观察结束时,DCa-1.5-Calcitriol,DCa-1.25+Calcitriol及DCa-1.25-Calcitriol组血清iPTH及BGP水平升高(P<0.05);DCa-1.25+Calcitriol及DCa-1.25-Calcitriol组血清Ca水平降低(P<0.05),Ca×P水平降低(P<0.05);DCa-1.5+Calcitriol组血清较同期DCa-1.25-Calcitriol组水平Ca水平增高(P<0.05);透前血清iPTH与BGP水平呈正相关(r=0.181,P<0.05)。结论生理浓度钙透析液能够减轻高钙负荷,持续有效刺激甲状旁腺素分泌及改善受抑制的骨代谢。联合骨化三醇及定期监测上述指标,可以安全有效的维持甲状旁腺素在适当水平不引发骨质疏松。     

Bone health and vascular calcification relationships in chronic kidney disease

Abnormal bone in chronic kidney disease (CKD) may adversely affect vascular calcification via disordered calcium and phosphate metabolism. In this context, bone health should be viewed as a prerequisite for the successful prevention/treatment of vascular calcification (VC) along with controlled parathyroid hormone (PTH) secretion, the use of calcium-based phosphate binders and vitamin D therapy. In CKD patients, VC occurs more frequently and progresses more rapidly than in the general population, and is associated with increased cardiovascular disease (CVD) morbidity and mortality. A number of therapies aimed at reducing PTH concentration are associated with an increase of calcaemia and Ca × P product, e.g. calcium-containing phosphate binders or active vitamin D. The introduction of calcium-free phosphate binders has reduced calcium load, attenuating VC and improving trabecular bone content. In addition, a major breakthrough has been achieved through the use of calcimimetics, as first agents which lower PTH without increasing the concentrations of serum calcium and phosphate. Nowadays, it is becoming evident that even early stage CKD is recognised as an independent CVD risk factor. Moreover, the excess of CVD among dialysis patients cannot be explained entirely on the basis of abnormal mineral and bone metabolism. Hence, much controversy has surrounded the cost-effectiveness of treatment with the new phosphate-binding drugs as well as new vitamin D analogs and calcimimetics. Thus, it seems prudent and reasonable that maintaining bone health and mineral homeostasis should rely on some modifications of standard phosphate binding and calcitriol therapy. Hypophosphataemia and hypercalcaemia in adynamic bone disease (ABD) might be treated by reducing the number of calcium carbonate/acetate tablets in order to increase serum phosphate and decrease serum calcium, which, in turn, might positively stimulate PTH secretion. The same rationale is assumed for the use of a low calcium dialysate. On the other hand, secondary hyperparathyroidism with hyperphosphataemia and hypocalcaemia should be treated with a substantial number of calcium carbonate/acetate tablets in combination with calcitriol and low calcium dialysate in order to decrease serum phosphate and maintain the Ca × P product within K/DOQI guidelines (<4.4 mmol l⁻¹). Finally, it becomes apparent that prevention, with judicious use of calcium-based binders, vitamin D and a low calcium dialysate without adverse effects on Ca × P or oversuppression of PTH, provides the best management of VC and mineral and bone disorder in CKD patients.     

Detection and quantification of cardiovascular calcifications with electron beam tomography to estimate risk in hemodialysis patients

Cardiovascular disease is the leading cause of death in dialysis patients, accounting for nearly half of all deaths among end-stage renal disease (ESRD) patients. Even young dialysis patients are at risk. Cardiovascular disease in chronic renal failure patients has been associated with elevated serum phosphorus levels and elevated calcium-phosphorus (Ca x P) product, and mismanagement of calcium and phosphorus metabolism has been implicated as a major factor in the development of soft tissue calcification and cardiovascular disease. ESRD patients frequently face hyperphosphatemia as well as excess calcium load, which elevate the Ca x P product, thereby contributing to the development of calcific complications. Electron beam computed tomography (EBCT) can be used to detect different calcification stages in a variety of tissues, and is a sensitive tool for detecting calcified coronary artery plaques as well as cardiac and valvular calcifications. Hemodialysis patients have high calcium scores on EBCT imaging, and these are associated with elevations in Ca x P product. In a recent study, patients with calcification were found to have had twice the daily calcium intake from calcium-based phosphate binders than patients without calcification. Strategies to reduce cardiac risk in hemodialysis patients include use of a dialysate low in calcium, use of vitamin D analogs that are less calcemic, and use of calcium-free phosphate binders. EBCT can be a useful adjunct to these therapies, since it permits sensitive and quantitative initial assessment, as well as ongoing monitoring of disease progression.     

Selective Cytopheretic Inhibitory Device With Regional Citrate Anticoagulation and Portable Sorbent Dialysis

Selective cytopheretic inhibitory device (SCD) therapy is an immunomodulatory treatment provided by a synthetic biomimetic membrane in an extracorporeal circuit, which has shown promise in preclinical large animal models of severe sepsis as well as in clinical trials treating patients with acute kidney injury and multiple organ failure. During SCD therapy, citrate is administered to lower ionized calcium levels in blood for anticoagulation and inhibition of leukocyte activation. Historically, citrate has been known to interfere with sorbent dialysis, therefore, posing a potential issue for the use of SCD therapy with a portable dialysis system. This sorbent dialysis SCD (sorbent SCD) would be well suited for battlefield and natural disaster applications where the water supply for standard dialysis is limited, and the types of injuries in those settings would benefit from SCD therapy. In order to explore the compatibility of sorbent and SCD technologies, a uremic porcine model was tested with the Allient sorbent dialysis system (Renal Solutions Incorporated, Fresenius Medical Care, Warrendale, PA, USA) and concurrent SCD therapy with regional citrate anticoagulation. The hypothesis to be assessed was whether the citrate load required by the SCD could be metabolized prior to recirculation from systemic blood back into the therapeutic circuit. Despite the fact that the sorbent SCD maintained urea clearance without any adverse hematologic events, citrate load for SCD therapy caused an interaction with the sorbent column resulting in elevated, potentially toxic aluminum levels in dialysate and in systemic blood. Alternative strategies to implement sorbent‐SCD therapy will be required, including development of alternate urease‐sorbent column binding chemistry or further changes to the sorbent‐SCD therapeutic circuit along with determining the minimum citrate concentration required for efficacious SCD treatment.     

Calcium mass transfer with dialysate containing 1.25 and 1.75 mmol/L calcium in peritoneal dialysis patients.

Studies with 1.75 mmol/L calcium dialysate have shown that patients gain calcium from dialysate. Thus, hypercalcemia, especially when calcium compounds are used for phosphate control, is a commonly seen complication. Dialysate with 1.25 mmol/L calcium has been available since 1989. Little is known about calcium mass transfer (CMT) with dialysate of this calcium concentration. CMT was measured in 20 stable adult peritoneal dialysis patients. Each CMT study consisted of a 2-L continuous ambulatory peritoneal dialysis (CAPD) exchange with a dwell time of 4 hours. CMT studies were performed using 1.25 and 1.75 mmol/L calcium dialysate with 1.5, 2.5, and 4.25 g/dL dextrose concentrations. CMT with 1.25 mmol/L calcium dialysate was compared to that with 1.75 mmol/L for each dextrose concentration. With a dextrose concentration of 1.5 g/dL, the mean CMT for 1.25 mmol/L calcium dialysate was -0.1 +/- 0.3 mmol versus 0.6 +/- 0.3 mmol for 1.75 mmol/L calcium dialysate (P < 0.0001). A dextrose concentration of 2.5 g/dL resulted in a mean CMT of -0.4 +/- 0.2 mmol for 1.25 mmol/L calcium versus 0.45 +/- 0.25 mmol for 1.75 mmol/L calcium (P < 0.0001). Using a dextrose concentration of 4.25 g/dL, the mean CMT was -0.7 +/- 0.25 mmol for 1.25 mmol/L calcium versus -0.05 +/- 0.35 mmol for 1.75 mmol/L calcium (P < 0.0001). Mean serum ionized calcium (SiCa) was between 1.15 and 1.20 mmol/L for all study groups. CMT inversely correlated with SiCa for each type of dialysate used. CMT was dependent on the concentrations of calcium and dextrose in the dialysate and the SiCa level at the time of the exchange.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dialysate bath and QTc interval in patients on chronic maintenance hemodialysis: pilot study of single dialysis effects

Introduction: Serum concentrations of potassium (K) and calcium (Ca) influence ionic currents and play an important role in the duration of ventricular action potential. Further, the influence of alkalosis in reducing ionized calcium has been well known for a long time. The aim of this study was to assess the effects of different dialysate electrolytes and bicarbonate concentrations on changes of QTc interval in patients on chronic hemodialysis. Methods: The study hemodialysis sessions were performed in 22 patients, with different electrolyte and bicarbonate concentrations in dialysate. Tested dialysate concentrations were K of 2 and 3 mmol/L; Ca 1.25, 1.5 and 1.75 mmol/L; and bicarbonate 30 and 34 mmol/L. An electrocardiogram (ECG) was recorded 1 hour before, at the end and every hour for 4 hours after each study dialysis session. QTc interval was measured from the beginning of the QRS complex to the end of a T wave on a 12-lead ECG. Blood was collected and K, total Ca, ionic Ca and pH evaluated. Results: At the end of the study hemodialysis session with dialysate containing low K (2 mmol/L), low Ca (1.25 mmol/L) and high bicarbonate concentration (34 mmol), mean QTc interval was significantly prolonged compared with that recorded with dialysate containing high K (3 mmol/L), high Ca (1.75 mmol/L) and bicarbonate (30 mmol) (40 ± 10 milliseconds vs. 2 ± 2 milliseconds; p<0.01). Dialysate with low concentration of low Ca, K and high concentration of bicarbonate was an independent predictor of QTc; the combination of low Ca and K and high bicarbonate strongly increased the risk of prolonged QTc interval. Conclusion: The present pilot study shows that changes in QTc interval during hemodialysis depend on both electrolyte and bicarbonate concentrations in dialysate.     

Sudden cardiac death in haemodialysis patients: Preventative options

Sudden cardiac death (SCD) is the most common cause of death in haemodialysis patients, accounting for 25% of all‐cause mortality. There are many potential pathological precipitants as most patients with end‐stage renal disease have structurally or functionally abnormal hearts. For example, at initiation of dialysis, 74% of patients have left ventricular hypertrophy. The pathophysiological and metabolic milieu of patients with end‐stage renal disease, allied to the regular stresses of dialysis, may provide the trigger to a fatal cardiac event. Prevention of SCD can be seen as a legitimate target to improve survival in this patient group. In the general population, this is most effective by reducing the burden of ischaemic heart disease. However, the aetiology of SCD in haemodialysis patients appears to be different, with myocardial fibrosis, vascular calcification and autonomic dysfunction implicated as possible causes. Thus, the range of therapies is different to the general population. There are potential preventative measures emerging as our understanding of the underlying mechanisms progresses. This article aims to review the evidence for therapies to prevent SCD effective in the general population when applied to dialysis patients, as well as promising new treatments specific to this population group.     

Increased risk of Staphylococcus epidermidis peritonitis in patients on dialysate containing 1.25 mmol/L calcium.

Peritoneal macrophage function is decreased in vitro in the presence of dialysate with 1.25 mmol/L calcium compared with that containing 1.75 mmol/L calcium. Theoretically, patients using this dialysate may have a higher risk of peritonitis. Nineteen patients on continuous ambulatory peritoneal dialysis (CAPD) or continuous cycling peritoneal dialysis (CCPD) were converted from dialysate with 1.75 mmol/L calcium (mean time, 33 +/- 26 months) to that with 1.25 mmol/L calcium, for some or all exchanges (mean time, 10 +/- 4.7 months). Peritonitis rates were compared with 19 control patients who remained on dialysate with 1.75 mmol/L calcium. The two groups were matched for the proportion of diabetics, sex, age, use of the Y-set, and dialysis modality (CAPD, CCPD). Peritonitis rates were similar in the study patients before conversion to 1.25 mmol/L calcium dialysate and in the control patients (0.49 v 0.58 episodes/patient-year, respectively). After conversion to dialysate with 1.25 mmol/L calcium, the peritonitis rate was 0.82 episodes/patient-year contrasted to 0.58 episodes/patient-year in the control patients (P = 0.09). The peritonitis rate due to Staphylococcus epidermidis was 0.51 episodes/patient-year when 1.25 mmol/L calcium dialysate was used, and 0.19 episodes/patient-year for the comparable period in the control patients on 1.75 mmol/L calcium dialysate (P = 0.005). The proportion of peritonitis episodes due to S epidermidis increased from 20% to 61% after conversion to 1.25 mmol/L calcium (P = 0.01). The increased risk of peritonitis due to S epidermidis in patients using dialysate with 1.25 mmol/L calcium is consistent with a previous study demonstrating that clearance of S epidermidis by peritoneal macrophages is less effective with a decrease in the dialysate calcium content.(ABSTRACT TRUNCATED AT 250 WORDS)     

低钙透析联合高通量透析对透析患者颈动脉钙化的影响

目的：探讨低钙透析联合高通量透析（ HFHD）对透析患者颈动脉钙化的影响。方法：将36例维持性血液透析（ MHD）患者随机分为A组（使用高通量透析器）和B组（使用低通量透析器）,两组均为低钙透析,共观察12个月。观察治疗前后两组颈动脉内-中膜厚度（IMT）、生化指标、血压、碳酸钙和活性维生素D3用量变化,记录不良反应。结果：（1） A组颈动脉IMT轻微增加,B组IMT明显增加,两组比较差异有统计学意义;（2）两组血钙、磷均有降低,A组较明显,B组甲状旁腺素（iPTH）明显升高,A组营养及炎症指标、血压改善优于B组;（3）两组碳酸钙及活性维生素D用量均增加;（4）无严重不良反应发生。结论：低钙透析联合高通量透析可改善血管钙化危险因素,延缓血管钙化的发生发展,可成为一种有效、安全且经济的治疗方法。