Lateral lumbar X-ray assessment of abdominal aortic calcification in Australian haemodialysis patients

Aim: Vascular calcification is prevalent in patients with chronic kidney disease. Abdominal aortic calcification (AAC) can be detected by X‐ray, although AAC is less well documented in anatomical distribution and severity compared with coronary calcification. Using simple radiological imaging we aimed to assess AAC and determine associations in prevalent Australian haemodialysis (HD) patients. Methods: Lateral lumbar X‐ray of the abdominal aorta was used to determine AAC, which is related to the severity of calcific deposits at lumbar vertebral segments L1 to L4. Two radiologists determined AAC scores, by semi‐quantitative measurement using a validated 24‐point scale, on HD patients from seven satellite dialysis centres. Regression analysis was used to determine associations between AAC and patient characteristics. Results: Lateral lumbar X‐ray was obtained in 132 patients. Median age of patients was 69 years (range 29–90), 60% were male, 36% diabetic, median duration of HD 38 months (range 6–230). Calcification (AAC score ≥ 1) was present in 94.4% with mean AAC score 11.0 ± 6.4 (median 12). Independent predictors for the presence and severity of calcification were age (P = 0.03), duration of dialysis (P = 0.04) and a history of cardiovascular disease (P = 0.009). There was no significant association between AAC and the presence of diabetes or time‐averaged serum markers of mineral metabolism, lipid status and C‐reactive protein. Conclusions: AAC detected by lateral lumbar X‐ray is highly prevalent in our cohort of Australian HD patients and is associated with cardiovascular disease, increasing age and duration of HD. This semi‐quantitative method of determining vascular calcification is widely available and inexpensive and may assist cardiovascular risk stratification.     

中晚期CKD患者腹主动脉钙化发生情况及危险因素分析

目的：分析中晚期CKD患者腹主动脉钙化的发生情况和危险因素。方法：63例透析及非透析CKD患者进行腹部侧位片的检查,分析腹主动脉钙化发生情况及影响因素。结果：中晚期CKD患者腹主动脉钙化发生率为54%;腹主动脉钙化与年龄、血磷水平、钙磷乘积和低密度脂蛋白水平呈正相关（P〈0.05）。结论：中晚期CKD患者腹主动脉钙化高发,远端起病,年龄、血脂、钙磷水平影响其程度。     

X线平片在诊断血液透析患者血管钙化中的应用

目的 评价X线平片检测维持性血液透析（MHD）患者动脉钙化的敏感性和特异性。 方法 54例MHD患者行腹部-股骨上1/3多层螺旋CT（MSCT）平扫及侧位腹平片、骨盆片X线检测。以腰椎（L）2～3间隙为界将腹主动脉分为上段、下段。MSCT结果据钙化严重程度分为0~5级。两位放射科医师分别盲法阅片诊断。以MSCT结果为金标准,X线平片结果作为诊断性指标,评价X线平片诊断腹主动脉和髂、股动脉钙化的敏感性和特异性。 结果 MSCT结果显示,腹主动脉钙化发生率为86.1%,髂、股动脉钙化发生率为74.5%,二者差异有统计学意义（χ2 = 5.695,P = 0.017）;腹主动脉2级以上钙化的发生率为60.2%,髂、股动脉为42.6%,腹主动脉钙化的严重程度显著高于髂、股动脉（χ2 = 8.922,P = 0.003）。X线平片结果表明,腹主动脉钙化发生率为51.9%,髂、股动脉钙化发生率为18.5%。X线平片诊断腹主动脉和髂、股动脉钙化的特异性均为100%,敏感性随MSCT动脉钙化程度的加重而增高。据MSCT钙化评分的不同,其诊断腹主动脉和髂、股动脉钙化的敏感性分别如下：≥1级：60.2%和24.8%;≥2级：76.9%和43.5%;≥3级：100%和74.4%。 结论 X线平片诊断中、重度动脉钙化敏感性高,诊断腹主动脉钙化的敏感度高于髂、股动脉,可用于MHD患者中、重度动脉钙化的检测。     

Assessment of vascular calcification in ESRD patients using spiral CT.

BACKGROUND: Dialysis patients have increased vascular calcification of the coronary arteries and aorta by electron beam CT scan. The purpose of the present study was to utilize an alternative machine, spiral CT, to assess calcification in end-stage renal disease (ESRD) patients. METHODS: Two groups of patients with ESRD were evaluated: group 1, those receiving a renal transplant (n=38); and group 2, those remaining on dialysis (n=33). All patients underwent quad-slice spiral CT with retrospective gating to evaluate coronary artery and aorta calcification scores. Both area (Agatston method) and volume calculations were utilized, with retrospective gating in all but 16 subjects. Laboratory tests, medications and clinical characteristics were analysed. RESULTS: Using spiral CT, the intra-reader variability for coronary artery calcification (after correction for very low scores) was 0.9% mean / 0% median using the area (Agatston method) and 2.9% mean / 0% median using volume calculations. Group 1 patients were younger, more likely to be Caucasian and on peritoneal dialysis, had lower serum calcium and higher C-reactive protein levels than group 2. In patients without vs those with coronary artery calcification, only longer duration of dialysis (34+/-64 vs 55+/-50 months, P=0.004; r=0.39, P=0.005) and increasing age (39+/-13 vs 54+/-10 years, P<0.001; r=0.29, P=0.039) were associated, whereas only increasing age was associated with aorta calcification. CONCLUSION: In ESRD patients, the factors correlating with coronary calcification were duration of dialysis and advancing age, whereas only age correlated with aorta calcification. Spiral CT offers an alternative technique for the assessment of these changes.     

Effects of Phosphate Binders in Moderate CKD

Some propose using phosphate binders in the CKD population given the association between higher levels of phosphorus and mortality, but their safety and efficacy in this population are not well understood. Here, we aimed to determine the effects of phosphate binders on parameters of mineral metabolism and vascular calcification among patients with moderate to advanced CKD. We randomly assigned 148 patients with estimated GFR=20-45 ml/min per 1.73 m(2) to calcium acetate, lanthanum carbonate, sevelamer carbonate, or placebo. The primary endpoint was change in mean serum phosphorus from baseline to the average of months 3, 6, and 9. Serum phosphorus decreased from a baseline mean of 4.2 mg/dl in both active and placebo arms to 3.9 mg/dl with active therapy and 4.1 mg/dl with placebo (P=0.03). Phosphate binders, but not placebo, decreased mean 24-hour urine phosphorus by 22%. Median serum intact parathyroid hormone remained stable with active therapy and increased with placebo (P=0.002). Active therapy did not significantly affect plasma C-terminal fibroblast growth factor 23 levels. Active therapy did, however, significantly increase calcification of the coronary arteries and abdominal aorta (coronary: median increases of 18.1% versus 0.6%, P=0.05; abdominal aorta: median increases of 15.4% versus 3.4%, P=0.03). In conclusion, phosphate binders significantly lower serum and urinary phosphorus and attenuate progression of secondary hyperparathyroidism among patients with CKD who have normal or near-normal levels of serum phosphorus; however, they also promote the progression of vascular calcification. The safety and efficacy of phosphate binders in CKD remain uncertain.     

Association of pulse wave velocity with vascular and valvular calcification in hemodialysis patients

The recent Kidney Disease: Improving Quality Outcomes (KDIGO) recommendations called for an investigation of the relationship between various radiological methods to assess cardiovascular calcification and measures of arterial stiffness. Accordingly, in 131 adult maintenance hemodialysis patients, we investigated the association of aortic pulse wave velocity (PWV) with calcification of cardiac valves on echocardiography, coronary artery, and thoracic aorta calcium on computed tomography and a calcification score of the abdominal aorta obtained on a plain abdominal X-ray. All tests were performed within a week. Mean PWV increased as the severity of coronary artery, thoracic, and abdominal aorta calcium scores increased (each P<0.05). No trend was present for number of valves with calcification. After multivariable adjustment, abdominal aorta X-ray calcium scores remained associated with PWV (P=0.004), whereas the association of PWV with thoracic aorta and coronary artery calcium scores became marginal (P=0.308 and P=0.083, respectively). No association was found between number of calcified valves and PWV. This study demonstrates a strong association between abdominal aorta calcification on plain X-ray and PWV and a borderline association with thoracic aorta and coronary artery calcification. Sudden death and congestive heart failure, two frequent causes of death in hemodialysis, are likely caused by increased arterial stiffness that can be closely predicted by the presence of aortic calcification on plain X-rays.     

Abdominal aorta and pelvic artery calcifications on plain radiographs may predict mortality in chronic kidney disease,hemodialysis and renal transplantation

Purpose

Vascular calcification is common in chronic kidney disease (CKD) and predicts poor patient outcomes. While computed tomography is the gold standard for evaluation of vascular calcification, plain radiograph offers a simpler and less costly alternative. The calcification of abdominal aorta, iliac and femoral arteries has been evaluated by plain radiograph, but the data on their outcome predictabilities are still limited. The present study investigated the role of abdominal aortic calcification (AAC) and pelvic arterial calcification (PAC) in predicting overall morality in non-dialysis CKD stages 2–5 (CKD 2–5), maintenance hemodialysis (HD) and long-term kidney transplant (KT) patients.

Methods

Four hundred and nineteen patients were included. Lateral abdominal and pelvic radiographs were obtained. The degree of AAC and PAC was evaluated according to the methods described previously by Kaupplia et al. and Adragao et al. Patients were followed prospectively for 5 years.

Results

AAC and PAC scores correlated well with the correlation coefficients of 0.442 for CKD 2–5, 0.438 for HD and 0.586 for KT (p < 0.001). Patients with AAC score > 6 or PAC score > 1 were older, showed higher prevalence of DM and had higher serum phosphate and PTH but lower serum albumin and eGFR. A more severe degree of AAC was associated with an increase in KT duration, whereas a more severe degree of PAC was associated with worsening kidney function and prolonged dialysis vintage. Kaplan–Meier survival curves revealed AAC score > 6 as a significant predictor of all-cause mortality in CKD 2–5 but not in HD or KT, whereas PAC score > 1 was a significant predictor of all-cause mortality in all three populations. After adjusting for age, the predictability of AAC was lost, whereas PAC remained an independent predictor of mortality in all three populations. Adjustments for cardiovascular and CKD risk factors including age, gender, BMI, DM, serum albumin, calcium and phosphate attenuated the predictability of PAC in HD but not in CKD 2–5 or KT patients.

Conclusion

PAC was better than AAC in predicting mortality in CKD, HD and KT patients.

     

Arteriosclerosis, vascular calcifications and cardiovascular disease in uremia

PURPOSE OF REVIEW: Arterial calcification in chronic kidney disease (CKD) is associated with increased cardiovascular risk. The mechanisms responsible for arterial calcification include alterations of mineral metabolism and expression of mineral-regulating proteins. RECENT FINDINGS: Arterial calcification is similar to bone formation, involving differentiation of vascular smooth muscle cells (VSMCs) into phenotypically distinct osteoblast-like cells. Elevated phosphate and/or calcium trigger a concentration-dependent increase of calcium precipitates in VSMC in vitro. The calcification is initiated by VSMC release of membrane-bound matrix vesicles and formation of apoptotic bodies. The presence of serum prevents these changes, indicating the presence of calcification inhibitors. Arterial calcification occurs in two sites: the tunica intima and tunica media. Intimal calcification is a marker of atherosclerotic disease and is associated with arterial stenotic lesions. Medial calcification influences outcome by promoting arterial stiffening whose principal consequences are left-ventricular hypertrophy and altered coronary perfusion. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in CKD patients. Age, duration of dialysis, smoking and diabetes are risk factors for the development of arterial calcification in end-stage renal disease. Oversuppression of parathyroid hormone and low bone turnover potentiate the development of arterial calcification. SUMMARY: Arterial disease in CKD patients is characterized by extensive calcification. Evidence has accumulated pointing to the active and regulated nature of the calcification process. Elevated phosphate and calcium may stimulate sodium-dependent phosphate cotransport involving osteoblast-like changes in cellular gene expression. Arterial calcification is responsible for stiffening of the arteries with increased left-ventricular afterload and abnormal coronary perfusion as the principal clinical consequences.     

Management of vascular calcification in CKD patients

Vascular calcification is common in patients with chronic kidney disease (CKD) and it may affect almost every artery. It is associated with a significant increase in morbidity and mortality. Therefore, the detection, prevention and treatment of vascular calcification in CKD patients are critical for the overall approach for the management of these patients. Hyperphosphatemia, especially when the blood levels of serum phosphorus are above 5.5 mg/dl, plays a major role in the development of vascular calcification. Hyperphosphatemia induces vascular calcification by both passive and active processes. By increasing calcium-phosphate product, hyperphosphatemia results in direct deposition of calcium salts in the arteries and in cardiac valves. The active process involves the uptake of phosphate by the smooth muscle cells of the arteries by a Na-P co-transporter. This increase in cell phosphate then induces phenotypic changes of these cells, rendering them into osteoblasts which in turn, begin laying calcium salts in the arterial walls. Therefore, it is critical that the blood levels of serum phosphorus be maintained below 5.5 mg/dl in CKD patients. Inflammation and the production of C-reactive protein (CRP) and interleukin 6 are also risk factors for vascular injury and vascular calcification. In a study of 254 dialysis patients with elevated blood levels of CRP (>1.0 mg/l) and 258 patients with CRP levels equal to or less than 1.0 mg/l, it was found that higher levels of CRP are significantly associated with the presence of both atheromatous and medial calcification of the aorta and hand arteries. Also, it was reported that a significant association between CRP levels and cardiac valves calcification in patients undergoing continuous ambulatory peritoneal dialysis. The reasons for the elevation in CRP in dialysis patients are not clear, but certainly, is more evident in those with obvious inflammatory processes. Therefore, any inflammation that is detected should be treated appropriately.     

Coronary calcification is associated with lower bone formation rate in CKD patients not yet in dialysis treatment

Vascular calcification is a strong prognostic marker of mortality in hemodialysis patients and has been associated with bone metabolism disorders in this population. In earlier stages of chronic kidney disease (CKD), vascular calcification also has been documented. This study evaluated the association between coronary artery calcification (CAC) and bone histomorphometric parameters in CKD predialysis patients assessed by multislice coronary tomography and by undecalcified bone biopsy. CAC was detected in 33 (66%) patients, and their median calcium score was 89.7 (0.4–2299.3 AU). The most frequent bone histologic alterations observed included low trabecular bone volume, increased eroded and osteoclast surfaces, and low bone‐formation rate (BFR/BS). Multiple logistic regression analysis, adjusted for age, sex, and diabetes, showed that BFR/BS was independently associated with the presence of coronary calcification [p = .009; odd ratio (OR) = 0.15; 95% confidence interval (CI) 0.036–0.619]. This study showed a high prevalence of CAC in asymptomatic predialysis CKD patients. Also, there was an independent association of low bone formation and CAC in this population. In conclusion, our results provide evidence that low bone‐formation rate constitutes another nontraditional risk factor for cardiovascular disease in CKD patients. © 2010 American Society for Bone and Mineral Research     

Evaluation of the role of severe hyperparathyroidism on coronary artery calcification in dialysis patients

BACKGROUND: Chronic kidney disease (CKD) patients are at a high risk of dying from a cardiovascular event, mainly due to coronary calcification. Among the various uremic and dialysis-specific risk factors for coronary calcification are mineral metabolism disorders. The role that secondary hyperparathyroidism (SHPT) consequent to the altered calcium and phosphate metabolism plays in the pathogenesis of coronary calcification remains unclear. The aim of this study was to evaluate the prevalence of coronary artery calcification in dialysis patients with severe SHPT submitted to multislice coronary tomography (MSCT) and to identify risk factors for coronary calcification. METHODS: This study involved 23 adult dialysis patients (age >18 years) with severe SHPT who were candidates for parathyroidectomy (PTX). All were submitted to MSCT and bone densitometry during the month preceding PTX. Fasting blood samples were collected immediately before surgery. Markers of mineral metabolism, including ionized calcium, phosphorus, alkaline phosphatase, intact-parathyroid hormone (iPTH), osteoprotegerin (OPG) and soluble receptor activator of nuclear factor-kappaB ligand, were analyzed. Dyslipidemia was assessed by determination of LDL, HDL and VLDL-cholesterol and triglyceride levels. Agatston units (AU) were used to calculate calcium scores. RESULTS: No coronary calcification was found in 30% of the patients. Moderate (calcium score > 100 AU) and severe (calcium score >400 AU) calcification was observed in 12 and 36% of the patients, respectively. In the univariate analysis, calcium volume correlated positively with VLDL-cholesterol (r = 0.44; p = 0.03) and, albeit less than significantly, with age (r = 0.35; p = 0.09), triglycerides (r = 0.39; p = 0.05) and Framingham risk index (r = 0.37; p = 0.07). We also found that OPG correlated negatively with bone mineral density at the L2-L4 lumbar vertebrae (r = -0.54; p = 0.007) and femoral neck (r = -0.43; p = 0.04). CONCLUSIONS: Although high levels of PTH should be considered a risk factor for cardiovascular death, the real role of severe SHPT on coronary calcification is to be clarified.     

Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients

BACKGROUND: Cardiovascular disease is frequent and severe in patients with end-stage renal disease. Disorders of mineral metabolism may contribute by promoting cardiovascular calcification. METHODS: We conducted a randomized clinical trial comparing sevelamer, a non-absorbed polymer, with calcium-based phosphate binders in 200 hemodialysis patients. Study outcomes included the targeted concentrations of serum phosphorus, calcium, and intact parathyroid hormone (PTH), and calcification of the coronary arteries and thoracic aorta using a calcification score derived from electron beam tomography. RESULTS: Sevelamer and calcium provided equivalent control of serum phosphorus (end-of-study values 5.1 +/- 1.2 and 5.1 +/- 1.4 mg/dL, respectively, P = 0.33). Serum calcium concentration was significantly higher in the calcium-treated group (P = 0.002), and hypercalcemia was more common (16% vs. 5% with sevelamer, P = 0.04). More subjects in the calcium group had end-of-study intact PTH below the target of 150 to 300 pg/mL (57% vs. 30%, P = 0.001). At study completion, the median absolute calcium score in the coronary arteries and aorta increased significantly in the calcium treated subjects but not in the sevelamer-treated subjects (coronary arteries 36.6 vs. 0, P = 0.03 and aorta 75.1 vs. 0, P = 0.01, respectively). The median percent change in coronary artery (25% vs. 6%, P = 0.02) and aortic (28% vs. 5%, P = 0.02) calcium score also was significantly greater with calcium than with sevelamer. CONCLUSIONS: Compared with calcium-based phosphate binders, sevelamer is less likely to cause hypercalcemia, low levels of PTH, and progressive coronary and aortic calcification in hemodialysis patients.     

CKD与非CKD患者冠状动脉钙化发生情况的比较研究

目的:比较CKD患者与非CKD患者的冠状动脉钙化情况。方法:选取473例曾在我院行冠脉CT检查的CKD及非CKD患者,通过收集其生化指标及冠脉CT检查结果,分析并比较两组患者冠状动脉钙化的发生情况。结果:CKD患者冠状动脉钙化的发生率为76.5%,且钙化累及分支更多,LAD、RCA多发。钙化组的尿素氮、血磷水平及钙磷乘积显著高于非钙化组,而GFR则显著低于非钙化组(P<0.01)。结论:CKD患者冠状动脉钙化发生率高,累及范围广,程度更重,且LAD、RCA钙化多发。钙化组的尿素氮、血磷水平及钙磷乘积显著高于非钙化组,而GFR则显著低于非钙化组。     

Association of pelvic arterial calcification with arteriovenous thigh graft failure in haemodialysis patients.

BACKGROUND: Arterial calcification is a common problem in patients with chronic kidney disease, and has been associated with adverse clinical outcomes. The goal of the present study was to evaluate whether pelvic artery calcifications are associated with technical failure of arteriovenous thigh grafts in haemodialysis patients. METHODS: From 1 January 1999 to 30 June 2002, thigh grafts were placed in 54 haemodialysis patients who had exhausted all options for permanent vascular access in the upper extremities. Perioperative computed tomography (CT) of the abdomen and pelvis was obtained in 32 of the patients for diagnostic purposes unrelated to vascular access planning. Two radiologists, who were blinded to the graft outcomes, scored the vascular calcifications on CT of the distal aorta, common iliac, external iliac and common femoral arteries on a semi-quantitative 5-point scale. The association between technical graft failure (inability to complete the anastomosis) and the vascular calcification score was analysed. RESULTS: There was a high inter-observer agreement in scoring vascular calcification (kappa = 0.801). Among 26 patients with absent or mild pelvic arterial calcifications (grade 1-2) on CT, none (0%) experienced technical graft failure. In contrast, three of six patients (50%) with moderate to severe calcification (grade 3-5) had technical graft failures (P = 0.004 by Fisher's exact test). The cumulative 1 year graft patency was lower in the group with grade 3-5 calcification (33 vs 81%, P = 0.09). The two groups were similar in age, gender, race, diabetes, duration of dialysis, serum calcium, serum phosphorus and serum parathyroid hormone. CONCLUSION: There is a strong association between pelvic artery calcifications and technical failure of thigh grafts. The presence of moderate to severe vascular calcification is predictive of poor cumulative 1 year graft patency.     

Pathogenesis and management of vascular calcification in CKD and dialysis patients

Patients with chronic kidney disease (CKD) have a predisposition to develop vascular calcification due to dysregulated homeostatic mechanisms, which lead to an imbalance in the circulatory promoters and inhibitors of vascular calcification, leading to a net calcification stress. These factors promote ectopic calcification and induce vascular smooth muscle cells to undergo osteogenic differentiation and actively calcify the vascular media. The article summarizes clinically relevant pathogenic mechanisms of vascular calcification in patients with CKD and in dialysis patients and summarizes novel therapeutic interventions. In addition to the management of traditional cardiovascular risk factors, patients with CKD‐mineral and bone disorder need close attention in the management of the mineral metabolism to prevent adverse effects on the bone and vascular compartments. This article reviews current evidence and therapeutic guidelines in the management of mineral metabolism in CKD and dialysis.     

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.     

Disturbances in Bone Largely Predict Aortic Calcification in an Alternative Rat Model Developed to Study Both Vascular and Bone Pathology in Chronic Kidney Disease

Because current rat models used to study chronic kidney disease (CKD)‐related vascular calcification show consistent but excessive vascular calcification and chaotic, immeasurable, bone mineralization due to excessive bone turnover, they are not suited to study the bone‐vascular axis in one and the same animal. Because vascular calcification and bone mineralization are closely related to each other, an animal model in which both pathologies can be studied concomitantly is highly needed. CKD‐related vascular calcification in rats was induced by a 0.25% adenine/low vitamin K diet. To follow vascular calcification and bone pathology over time, rats were killed at weeks 4, 8, 10, 11, and 12. Both static and dynamic bone parameters were measured. Vascular calcification was quantified by histomorphometry and measurement of the arterial calcium content. Stable, severe CKD was induced along with hyperphosphatemia, hypocalcemia as well as increased serum PTH and FGF23. Calcification in the aorta and peripheral arteries was present from week 8 of CKD onward. Four and 8 weeks after CKD, static and dynamic bone parameters were measurable in all animals, thereby presenting typical features of hyperparathyroid bone disease. Multiple regression analysis showed that the eroded perimeter and mineral apposition rate in the bone were strong predictors for aortic calcification. This rat model presents a stable CKD, moderate vascular calcification, and quantifiable bone pathology after 8 weeks of CKD and is the first model that lends itself to study these main complications simultaneously in CKD in mechanistic and intervention studies. © 2015 American Society for Bone and Mineral Research.     

慢性肾脏疾病3～5期患者腹主动脉钙化的发生情况及影响因素分析

目的通过研究湖北地区慢性肾脏疾病（chornic kidney diseases,CKD）3～5期患者腹主动脉钙化的发生情况及影响因素,为CKD中晚期出现血管钙化的患者的提供临床诊疗依据。方法将123例患者按CKD不同分期分为CKD3期组、CKD4期组和CKD5期组,收集所有患者的一般资料,包括性别、年龄、身高、体质量、体质量指数（bodymassindex,BMI）、高血压病史及糖尿病病史;比较各组患者的血肌酐、白蛋白、前白蛋白、总胆固醇（total cholesterol,TC）、三酰甘油（triglyc—eride,TG）、高密度脂蛋白胆固醇（high density lipoprotein cholesterol,HDL-C）、低密度脂蛋白胆固醇（low density lipoprotein cholesterol,LDL-C）、空腹血糖、血钙、血磷、甲状旁腺素（parathyroidhor—mone,PTH）及超敏C反应蛋白（high sensitive c-reactive protein,hs-CRP）的水平,并评估腹主动脉钙化的发病率及其相关影响因素。结果CKD3期组血磷、钙磷乘积及PTH水平高于CKD4期组和CKD5期组（P〈0．01,P〈0．05）,而血钙水平低于CKD4期组,但无统计学差异（P〉0．05）,与CKD5期组比较,有统计学差异（P〈0．05）;CKD5期组血钙与CKD4期组比较有统计学意义（P〈0．05）;其余实验室指标在CKD各期组比较均无统计学意义（P〉0．05）。根据患者有无腹主动脉钙化将其分为腹主动脉钙化组和非钙化组,2组的年龄和hs—CRP相比有统计学意义（P〈0．01,P〈0．05）;以腹主动脉钙化为因变量,将年龄、高血压病史发病率及hs—CRP三项因素进行logistic相关性分析,结果显示年龄与腹主动脉钙化有统计学意义。结论年龄为CKD3～5期患者腹主动脉钙化的独立影响因素,而hs—CRP和高血压发病率也是影响CKD患者腹主动脉钙化的重要因素。     

应用腰椎侧位片评价血液透析患者腹主动脉钙化

目的 应用X线平片腹主动脉钙化评分探讨维持性血液透析( MHD)患者腹主动脉钙化患病率和相关危险因素分析.方法 选取我院资料完整的155例MHD患者为研究对象.通过X线腰椎侧位片检测腹主动脉钙化( AAC)并对其进行评分.结果 155例的腰椎侧位片中,腹主动脉钙化主要发生在第4腰椎节段,并随着节段的上升而逐渐减少.63.63％患者的侧位平片上可见腹主动脉钙化;28.39％患者可见严重腹主动脉钙化(钙化累及3个节段以上).MHD患者的年龄(OR=1.094,P＜0.01)、透析龄(OR=1.013,P=0.022)、血三酰甘油(OR=1.261,P=0.030)和血磷(OR=1.324,P=0.023)水平是发生腹主动脉钙化的独立危险因素,而白蛋白(OR=0.239,P=0.013)为保护性因素.结论 MHD患者腹主动脉钙化患病率高,且与多个血管钙化因素相关.半定量的X线腰椎侧位片方法价格便宜、操作简便,易于临床推广.其对MHD患者的预测价值有待日后更多的随访研究.