Left ventricular mass index and aortic arch calcification score are independent mortality predictors of maintenance hemodialysis patients

To analyze predictive factors for all‐cause mortality, cardiovascular (CV) mortality, nonfatal CV events (CVE) in maintenance hemodialysis (MHD) patients, and to compare the effects of standard hemodialysis (HD) and online hemodiafiltration (HDF) on these factors and outcomes. A total of 333 MHD patients were prospectively followed up for 50 ± 15 months and all‐cause death, CV death and CVE were registered. At the baseline, demographic, clinical, and laboratory data of the whole population were recorded. Then, patients were stratified into two groups according to the dialysis modalities, HD (n = 268) and HDF (n = 65). At the end of 6th month, clinical and laboratory data were recorded again. The predictive factors at baseline for all‐cause mortality, CV mortality, and CVE were analyzed by Cox regression. The effects of HD and HDF on these factors at the 6th month and long‐term outcomes were compared by t‐test and Kaplan–Meier method, respectively. Age, gender, left ventricular mass index (LVMI), aortic arch calcification score (AoACS), hemoglobin (Hb) <10 g/dL, and ferritin >500 ng/mL maintained independent associations with all‐cause mortality. C‐reactive protein (CRP), LVMI, AoACS, and Hb <10 g/dL were associated with CV mortality. Prior cardiovascular disease (CVD), AoACS and LVMI were independent predictors of nonfatal CVE. Higher body mass index (BMI), body weight, total serum cholesterol, Hb concentration, and lower CRP level, LVMI, and AoACS were found in patients on HDF at the end of the 6th month. Improved outcomes with longer survival time for all‐cause mortality, CV mortality, and CVE were found in HDF group. Age, gender, LVMI, AoACS, Hb, and ferritin were predictors of all‐cause mortality in MHD patients. CRP, LVMI, AoACS, and Hb were associated with CV mortality. Prior CVD, AoACS, and LVMI were independent predictors of nonfatal CVE. HDF could improve BMI, body weight, total serum cholesterol, Hb, CRP, LVMI, AoACS, and long‐term outcomes, including all‐cause mortality, CV mortality, and CVE.     

A dynamicin vitro method for studying bioprosthetic heart valve calcification

The most predictable cause of failure of a biological prosthetic heart valve is calcification. The deposition process appears to be related both to the biomaterial composition and to the presence of dynamic stresses in the leaflets. A dynamicin vitro test has been developed to investigate the calcification process. The test apparatus consists of a modified Rowan Ash fatigue tester with the test fluid maintained at 37°C. Six valves can be tested simultaneously under similar physical conditions, but with individual incubation media. The valves tested were glutaraldehyde-fixed bovine pericardial valves (the Glasgow Heart Valve). These have been tested in a range of different simple salt solutions containing approximately physiological concentrations of calcium and phosphate. Calcification has been analysed by assay of the incubation media for depletion of calcium and phosphate and direct measurement of uptake of calcium by the valves. There is a wide variability among pericardial valves treated similarly. This may be related to the variability in calcification rate seen in patients with valve implants.     

Effect of serum FGF‐23, MGP and fetuin‐A on calcium‐phosphate metabolism in maintenance hemodialysis patients

This study was aimed to explore the role of serum fibroblast growth factor (FGF)‐23, matrix Gla protein (MGP) and fetuin‐A in the calcium‐phosphate metabolism and their predicting value in coronary artery calcification in maintenance hemodialysis (MHD) patients. This study included 64 patients who receive hemodialysis in our hospital. The serum FGF‐23, MGP and fetuin‐A were analyzed by enzyme‐linked immunosorbent assay (ELlSA). Coronary artery calcification score (CACS) was evaluated by coronary artery computed tomography scan. The 64 patients (30 males, 34 females, 60.6 ± 11.3 years of age) received an average dialysis vintage of 6.88 ± 2.94 years. We divided the CACS into three levels, and 13 (20.31%), 16 (25%), and 35 (54.69%) exhibited a CACS of 0–100, 100–400, and >400, respectively. Dialysis vintage, serum FGF‐23, fetuin‐A, phosphorus and high‐density lipoprotein‐C levels were identified as independent variables of CACS by stepwise multiple regression analysis. The area under receiver operating characteristic curve indicated that serum FGF‐23 and fetuin‐A were useful for identifying CAC in MHD patients. The cut‐off value corresponding to the highest Youden's index was serum FGF‐23 ≥ 256 pg/mL and fetuin‐A ≤ 85 μg/mL, which was defined as the optimal predictors of CAC. Different combinations of serum FGF‐23 and fetuin‐A in parallel or in series effectively boosted the identification of CAC. The incidence of CAC is high in MHD patients. Serum FGF‐23 and fetuin‐A levels are closely correlated with CAC.     

Both pelvic radiography and lateral abdominal radiography correlate well with coronary artery calcification measured by computed tomography in hemodialysis patients: A cross‐sectional study

Introduction Lateral abdominal radiograph is suggested as an alternative to coronary artery computed tomography (CT) in evaluating vascular calcification. Simple scoring systems including pelvic radiograph scoring and abdominal scoring system were utilized to study their correlation with coronary artery calcification. Methods In 106 MHD patients, coronary artery CT, lateral abdominal, and pelvic radiograph were taken. The Agatston scoring system was applied to evaluate the degree of coronary artery calcification which was categorized according to Agatston coronary artery calcification score (CACS) ≥ 30, ≥100, ≥400, and ≥1000. Abdominal aortic calcification was scored by 4‐scored and 24‐scored systems. Pelvic artery calcification was scored by a 4‐scored system. Sensitivities and specificities of abdominal aortic calcification scores and pelvic artery calcification scores to predict different categories of coronary artery calcification were analyzed. We studied the diagnostic capability of abdominal aorta calcification and pelvic artery calcification to predict different CACS categories by calculating likelihood ratios. Receiver operator characteristic curves were used to determine the area under the curve for each of these testing procedures. Findings The prevalence was 48(45.3%), 15 (14.2%), 11 (10.4%), 11 (10.4%), and 11 (10.4%) for CACs > 0, ≥30, ≥100, ≥400, and ≥1000, respectively. The degree of CACs was positively correlated with patient age, prevalence of diabetes, abdominal aorta scores, and pelvic calcification scores. The areas under the curves for different CACS by all X‐ray scoring systems were above 0.70 except pelvic 4‐scored system for diagnosing CACS ≥30, without significant difference (P > 0.05). Discussion Both lateral abdominal and pelvic plain radiographs were demonstrated as acceptable alternatives to CT in evaluating vascular calcification.     

Poor correlation between coronary artery calcification and obstructive coronary artery disease in an end-stage renal disease patient

Vascular calcification is highly prevalent and often severe in patients with chronic kidney disease. Arterial calcification in patients with chronic kidney disease can result from the deposition of mineral along the intimal layer of arteries in conjunction with atheromatous plaques or from calcium deposition in the medial wall of arteries, also known as Monckeberg's sclerosis. Whether coronary artery calcium scores as measured by electron beam computed tomography correlate with occlusive atherosclerotic disease in the dialysis population is uncertain. Here we report a case of an asymptomatic patient with diabetes mellitus and end-stage renal disease undergoing maintenance hemodialysis, who was found to have extremely elevated coronary artery calcium scores on electron beam computed tomography, but varied degrees of atherosclerotic plaque in her coronary arteries on coronary angiography. This suggests that in addition to the calcification anticipated in a remodeled intima, a proportion of the calcification is also likely to be in the arterial media. Thus, this case demonstrates that even an extremely high coronary calcium score may not be a satisfactory surrogate marker for obstructive atherosclerosis in elderly diabetic dialysis patients.     

Impact of coronary artery calcification in hemodialysis patients: Risk factors and associations with prognosis

The risk factors of coronary artery calcification (CAC) and the impact of CAC on cardiovascular events, cardiovascular deaths, and all‐cause deaths in hemodialysis (HD) patients have not been fully elucidated. We examined the CAC score (CACS) in 74 HD patients using electron‐beam computed tomography. Fifty‐six patients underwent a second electron‐beam computed tomography after a 15‐month interval to evaluate CAC progression. We evaluated (1) the risk factors for CAC and its progression and (2) the impact of CAC on the prognosis. In the cross‐sectional study, HD vintage and high‐sensitive C‐reactive protein (hsCRP) were the independent risk factors for CAC. In the prospective cohort study, delta CACS (progression of CAC) was significantly correlated with hsCRP, fibrinogen, and serum calcium level in the univariate analysis. Stepwise multiple regression analysis revealed that only hsCRP was the independent risk factor for CAC progression in HD patients. Kaplan‐Meier survival analysis revealed that cardiovascular events (P<0.0001), cardiovascular deaths (P=0.039), and all‐cause deaths (P=0.026) were significantly associated with CACS. In conclusion, CAC had significantly progressed in HD patients during the 15‐month observation period. Microinflammation was the only independent risk factor for CAC progression in HD patients. The advanced CAC was a significant prognostic factor in HD patients, i.e., which was strongly associated with future cardiovascular events, cardiovascular deaths, and all‐cause deaths.     

Treatment of a soft tissue calcification in a patient receiving peritoneal dialysis

Chronic Kidney Disease patients suffer from Mineral and Bone Disorder (CKD‐MBD) leading to increased vascular and soft‐tissue calcification. The prevalence of soft tissue calcification in dialysis patients is not well described, and most cases describe such calcifications in hemodialysis patients. We describe a case of a massive soft tissue calcification in the right gluteal region in a peritoneal dialysis patient. The patient had severe pain and were disabled. The treatment was converted to an intensive hemodialysis regimen with a minimal calcium load and high dose of cinacalcet. During the treatment, the calcification diminished rapidly from a diameter of 26.6 to 2.9 cm, and the patient symptoms were relieved, leaving the patient with no pain or restriction in mobilization.     

Malnutrition‐inflammation‐coronary calcification in pediatric patients receiving chronic hemodialysis

Malnutrition, inflammation, and renal osteodystrophy parameters with resultant coronary calcification (CC) are associated with increased cardiovascular mortality in adults. Previous pediatric studies demonstrated CC in children but none assessed for an association between inflammation, malnutrition, renal osteodystrophy, and CC. To assess CC, ultrafast computerized tomogram was obtained for 16 pediatric patients (6 females; median age 17.2 years; range 9.1–21.2 years) receiving hemodialysis for ≥2 months. Inflammation was assessed by serum IL‐6, IL‐8, and C‐reactive protein levels on the day of the computerized tomogram scan; nutrition parameters included serum albumin, cholesterol, the body mass index standard deviation score, and normalized protein catabolic rate. Renal osteodystrophy parameters included time‐averaged serum calcium, phosphorus, total PTH, and calcitriol/calcium dose. Patients received hemodialysis thrice‐weekly; mean single pool Kt/V 1.48±0.13; and mean normalized protein catabolic rate 1.27±0.17 g/kg/day. Five of 16 patients had CC. Patients with CC were older (19.1±2.1 vs. 15.4±3.1 months; P=0.03), had longer dialysis vintage (49.4±15.3 vs. 17.2±10.5 months, P=0.0002), lower serum cholesterol (122±17.7 vs. 160.4±10.6 mg/dL, P=0.02), and higher phosphorus (9.05±1.2 vs. 6.1±0.96 mg/dL, P=0.0001). Mean serum albumin and normalized protein catabolic rate did not differ for patients with CC. All patients had elevated IL‐6 and IL‐8 levels compared with healthy norms; the mean IL‐6, IL‐8, and C‐reactive protein levels were not different in patients with CC. Coronary calcification was prevalent in older children receiving maintenance hemodialysis with a longer dialysis vintage. Worse renal osteodystrophy control and malnutrition (low cholesterol) may contribute to CC development.     

Factors associated with serum magnesium and vascular stiffness in maintenance hemodialysis patients

Introduction : We evaluated the associated factors of serum magnesium in patients on maintenance hemodialysis (MHD). Furthermore, we evaluated the relationship between low serum magnesium and arteriosclerosis in these patients. Methods : In 129 patients on MHD, we evaluated the blood levels of magnesium, brachial‐ankle pulse wave velocity (ba‐PWV), ankle‐brachial index (ABI), and intima‐media thickness of the common carotid artery (IMT). Findings : In MHD patients, the serum level of magnesium was significantly correlated with age, calcium, TNF‐α, albumin, and ba‐PWV but not with ABI or IMT. In the multiple regression analysis, albumin (P = 0.0001, β = 0.31) and calcium (P = 0.029, β = 0.18) were selected as significant predictors of the magnesium level in MHD patients. Furthermore, the serum level of magnesium, as well as systolic blood pressure (P = 0.0001, β = 0.32) and age (P = 0.005, β = 0.25), were selected as significant (P = 0.012, β = ?0.22) predictors of ba‐PWV in MHD patients. Discussion : In MHD patients, the serum magnesium level was associated with the serum levels of calcium and albumin. Furthermore, a low serum magnesium level in MHD patients was associated with the index of vascular stiffness.     

Calcium-sensing receptor gene polymorphisms and cardiac valvular calcification in patients with chronic renal failure: A pilot study

Cardiac valvular calcification (VC) is a frequent finding in chronic hemodialysis patients. In addition to demographic and metabolic factors, genetic susceptibility may also influence the occurrence and severity of these abnormalities and account for interindividual variability among patients. In this report, we studied the relation of calcium-sensing receptor (CaSR) gene polymorphisms to the development of VC in chronic hemodialysis patients. A total of 41 chronic hemodialysis patients (26 male, mean age 47.23 ± 11.36 years vs. 15 females, mean age 48.13 ± 14.66 years) undergoing treatment for more than 1 year were evaluated with transthoracic echocardiography. In patients with and without VC, CaSR gene polymorphisms (A990G, C1011G) were investigated by PCR, using allele-specific primers. In randomly chosen subjects, PCR analysis was verified by DNA sequencing. Cardiac valve calcification was detected in 21 patients (51.2%). Five of these patients (12.2%) had mitral valve calcification, 4 (9.75%) had aortic valve calcification, and 12 (29.27%) had both. In patients with VC, the frequency of the A/G genotype was slightly higher than those with no VC with a borderline P value (42.9% vs. 15%, χ²=3.840, P=0.050). The frequency of the C/C genotype was similar in patients with and without VC (90.5% vs. 85%, P>0.05). The results of this study are not enough to prove the role of CaSR gene polymorphisms in the development of VC. There is a need for large-scale studies on this topic.     

Enhanced expression of hemoglobin scavenger receptor and heme oxygenase‐1 is associated with aortic valve stenosis in patients undergoing hemodialysis

A high prevalence and a rapid progression of aortic valve stenosis (AS) in patients undergoing hemodialysis (HD) has been reported. In these circumstances, intraleaflet hemorrhage of aortic valve may be related to the development of AS in HD patients. We immunohistochemically examined the relationship among intraleaflet hemorrhage, neovascularization, hemoglobin scavenger receptor (CD163), and heme oxygenase‐1 (HO‐1) using surgically resected aortic valve specimens from AS patients undergoing HD. The study population consisted of 26 HD patients and 25 non‐HD patients with severe AS who had undergone aortic valve replacement. Frozen aortic valve samples surgically obtained from AS patients were stained immunohistochemically with antibodies against smooth muscle cells, macrophages, glycophorin‐A (a protein specific to erythrocyte membranes), CD31, CD163, and HO‐1. Morphometric analysis demonstrated that the CD163‐positive macrophage score, the number of CD31‐positive microvessels, and the percentage of glycophorin‐A and HO‐1‐positive area were significantly higher in HD patients than in non‐HD patients (CD163‐positive macrophage score, P < 0.0001; CD31‐positive microvessels, P < 0.0001; glycophorin‐A, P < 0.0001; HO‐1, P < 0.0001). Double immunostaining for CD163 or HO‐1 and macrophages revealed that the majority of CD163‐ or HO‐1‐positive cells were macrophages. Furthermore, CD163‐positive macrophage score was positively correlated with glycophorin‐A, HO‐1‐positive area, and the number of CD31‐positive microvessels (glycophorin‐A, R = 0.66, P < 0.0001; HO‐1, R = 0.50, P < 0.0005; microvessels, R = 0.38, P < 0.01). These findings suggest a positive association among intraleaflet hemorrhage, neovascularization, and enhanced expression of CD163 and HO‐1 as a response to intraleaflet hemorrhage in stenotic aortic valves in AS patients undergoing HD.     

Risk factors for progression of aortic arch calcification in patients on maintenance hemodialysis and peritoneal dialysis

Vascular calcification is accelerated during dialysis and is known to be an important risk factor for cardiovascular disease. Progression of aortic arch calcification (AoAC) can be simply estimated with an AoAC score (AoACS) using plain chest radiography. The objective of this study was to evaluate risk factors for AoAC progression. The enrolled subjects were 125 newly treated hemodialysis patients and 59 peritoneal dialysis patients. In the patients who had undergone chest radiography before initial dialysis therapy and every year, we estimated AoACS and then divided the patients into two groups based on the presence or absence of AoAC progression. We also compared the baseline clinical and biochemical profiles in the two groups. Eighty‐five (46.2%) were men (mean age, 58.6 ± 12.7 years). Seventy‐six patients (41.3%) had AoAC before initial dialysis, with a mean AoACS of 13.0 ± 20.4%. The mean duration of follow‐up was 2.7 ± 1.0 years. Half of the patients (50%) had progressive AoAC. Age >65 years (p = 0.003), dialysis duration (p = 0.004), diabetes (p = 0.015), and the presence of AoAC at baseline (p = 0.001) were related to AoAC progression. No significant association was found between AoAC progression and the baseline clinical parameters, including gender, obesity, hypertension, and dialysis modality. In a multivariate analysis, dialysis duration (p = 0.003) and the presence of AoAC at baseline (p < 0.001) were independent risk factors for AoAC progression in patients undergoing dialysis. The duration of dialysis and the presence of AoAC before initial dialysis were significantly related to the progression of AoAC in these patients. The results suggest that patients should be carefully managed from the predialysis stage to prevent AoAC progression and to reduce cardiovascular morbidity.     

Association of serum alkaline phosphatase and bone mineral density in maintenance hemodialysis patients

Recent studies indicate that serum alkaline phosphatase (AlkPhos), a surrogate of high turnover bone disease, is associated with coronary artery calcification and death risk in maintenance hemodialysis (MHD) patients. The association between AlkPhos and bone mineral density (BMD) is not well studied. We studied the association between AlkPhos and dual‐energy X‐ray absorptiometry‐assessed BMD in a group of MHD patients in Southern California. In 154 MHD patients, aged 55.3 ± 13.6 years, including 42% women, 38% Hispanics, 42% African Americans, and 55% diabetics, the mean serum AlkPhos was 121 ± 63 U/L (median: 101, Q_25–75: 81–141); 36% had AlkPhos≥120 U/L and 50% had a total T‐score≤?1. Whereas the total BMD did not correlate with age (r=0.01, P=0.99) or body mass index (r=0.10, P=0.22), it correlated negatively with AlkPhos (r=?0.25, P=0.002), including after multivariate adjustment (r=?0.24, P=0.003). The proportion of patients with a high coronary artery calcification score>400 was incrementally higher across worsening BMD tertiles (P trend=0.04). The BMD was significantly worse in MHD patients with serum AlkPhos≥120 U/L compared with <120 U/L (1.01 ± 0.016 vs. 1.08 ± 0.013 g/cm², respectively, P<0.001). The multivariate adjusted odds ratio of AlkPhos≥120 U/L for having a total T‐score相似文献   

Dialysate calcium and calcium/phosphate balance in hemodialysis

The changing pattern of pharmaceutical use in dialysis patients has resulted in several alterations to dialysate calcium concentration over the past 40 years. Non‐calcium–containing phosphate binders and calcimimetics are the most recent examples of drugs that influence the overall calcium balance in dialysis patients. Renal osteodystrophy, vascular disease, and mortality are believed to be linked in patients with chronic kidney disease (CKD), although to date most of the evidence is based only on statistical associations. The precise pathophysiology of vascular calcification in end‐stage renal disease is unknown, but risk factors include age, hypertension, time on dialysis, and, most significantly, abnormalities in calcium and phosphate balance. Prospective studies are required before “cause and effect” can be established with certainty, but it is an active metabolic process with inhibitors and promoters. Serum calcium levels are clearly influenced by dialysate calcium and may therefore play an important role in influencing vascular calcification. Clinical management of hyperphosphatemia is being made easier by the introduction of potent non‐calcium–based oral phosphate binders such as lanthanum carbonate. Short‐term and long‐term studies have demonstrated its efficacy and safety. Vitamin D analogs have been a disappointment in the control of serum parathyroid hormone (PTH) levels, but evidence is emerging that vitamin D has other important metabolic effects apart from this, and may confer survival advantages to patients with CKD. Calcimimetics such as cinacalcet enable much more effective and precise control of PTH levels, but at the cost of a major financial burden. While it is unreasonable to expect that any one of these recent pharmacological developments will be a panacea, they provide researchers with the tools to begin to examine the complex interplay between calcium, phosphate, vitamin D, and PTH, such that further progress is fortunately inevitable.     

Treatment of severe metastatic calcification in hemodialysis patients

Soft tissue and vascular calcifications are commonly present in uremic patients secondary to disturbances in calcium and phosphate balance and secondary to hyperparathyroidism. We report a uremic patient who developed uncontrolled hyperparathyroidism rapidly within 6 months after commencing hemodialysis (HD) therapy, with clinical presentations of tumoral calcinosis, calciphylaxis, and myocardial calcifications. After treatment with a low-calcium dialysate, non–calcium-containing phosphate binders, and parathyroidectomy, a dramatic resolution of soft tissue calcification was achieved. However, there was relatively little change in the vascular and other visceral calcifications over the 3-month observation period. This case highlights an unusual and rapid development of tertiary hyperparathyroidism, the importance of tight calcium/phosphate control in uremic patients, the potential hazards of a high calcium concentration dialysate, and the dangers of the overzealous use of active vitamin D therapy in HD patients with uncontrolled hyperparathyroidism.     

Coronary and aortic calcifications in patients new to dialysis

Background: Vascular calcification has been associated with all cause and cardiovascular mortality in patients with end‐stage kidney disease (ESRD). Whether vascular calcification is present in persons with advanced chronic kidney disease starting dialysis or develops in patients on dialysis is unknown. The purpose of this study was to examine the prevalence of vascular and coronary calcification in patients new to hemodialysis. Methods: A total of 129 subjects new to dialysis were evaluated using electron beam computed tomography. The primary outcome was the presence and extent of coronary artery, aortic, and valvular calcification. Results: Forty‐three percent of subjects had no significant coronary artery calcification (total score ≤ 30) and 27% had no detectable aortic calcification. Thirty‐four percent had coronary artery scores that placed them above the 90th percentile for age and sex. Coronary artery calcification was significantly associated with a history of coronary artery disease and atherosclerotic vascular disease (ASVD) whereas aortic calcification was significantly associated with ASVD. Age (p < 0.0001), pulse pressure (p = 0.004), diabetes mellitus (p = 0.009), and a history of smoking (p = 0.026) were independently associated with the extent of coronary artery calcification. Age (p < 0.0001) and pulse pressure (p = 0.0003) were independently associated with the extent of aortic calcification. Conclusions: A large fraction of patients new to hemodialysis had no evidence of coronary artery or aortic calcification. Coupled with the extensive vascular calcification reported by others in prevalent dialysis patients these findings suggest that dialysis‐specific factors contribute to calcific vascular disease in ESRD.     

Cervical tumoral calcinosis with secondary hyperparathyroidism in a chronic hemodialysis patient

Tumoral calcinosis is an uncommon and severe complication of chronic renal failure. It is generally associated with the presence of a high‐serum calcium‐and‐phosphorus product. We report here a case of a patient on maintenance hemodialysis who presented with progressively increasing, solitary, tumor‐like swelling over the nape of the neck. A 50‐year‐old female on thrice weekly maintenance hemodialysis for the last 3 years presented with a small swelling over the nape of the neck that had been progressively increasing over the last 1 year to cricket ball size. The patient was investigated and diagnosed as having tumoral calcinosis. The metastatic calcification occurring in the patient was most likely related to high calcium × phosphate product with coexistent secondary hyperparathyroidism possibly aggravated by vitamin D therapy. The patient was treated with withdrawal of vitamin D therapy, strict control of serum phosphate levels with noncalcemic phosphate binders, and subtotal parathyroidectomy. The neck swelling started decreasing in size after 2 months of parathyroidectomy and there was marked clinical improvement with drop in serum parathormone levels, over a period of 6 months. After 2 years of parathyroidectomy, the neck swelling again started increasing in size with increase in serum parathormone levels. The patient was treated with cinacalcet and the neck swelling gradually decreased in size along with control of serum parathormone and phosphate levels.     

Integration of clinical and imaging data to predict death in hemodialysis patients

In a prior publication, we demonstrated that a model integrating clinical and simple imaging data predicted the presence and severity of coronary artery calcification in prevalent hemodialysis patients. Herein we report the ability of the same model to predict all‐cause death. We assessed all‐cause mortality in 141 consecutive maintenance hemodialysis patients from two dialysis centers followed for a median of 79 months from enrollment. Patients were risk stratified according to a simple cardiovascular calcification index (CCI) that included patient's age, dialysis vintage, calcification of the cardiac valves, and abdominal aorta. The mean patients’ age was 55 ± 14 years. Abdominal aorta calcification was present in 57% of the patients, and 44% and 38% had aortic and mitral valve calcification, respectively. During follow‐up, 75 deaths (93 deaths per 1000 person‐years) were recorded. The CCI was linearly associated with risk of death, such that the unadjusted hazard risk (HR) increased by 12% for each point increase in CCI (P < 0.001). Further adjustments for age, sex, study center, diabetes mellitus, history of cardiovascular disease, hypertension, congestive heart failure, left ventricular hypertrophy, systolic, and diastolic blood pressure did not substantially change the strength of this association (HR 1.10; 95%CI: 1.00–1.21; P = 0.03). The CCI is a simple clinical model that can be used to risk stratify maintenance hemodialysis patients.     

The relationship between neutrophil‐to‐lymphocyte ratio and vascular calcification in end‐stage renal disease patients

Chronic inflammation was found to be correlated with coronary (CAC) and thoracic peri‐aortic calcification (TAC) in end‐stage renal disease (ESRD) patients. Neutrophil‐to‐lymphocyte ratio (NLR) was introduced as a potential marker to determine inflammation in cardiac and noncardiac disorders. Data regarding NLR and its association with TAC and CAC are lacking. We aimed to determine the relationship between NLR and vascular calcification in ESRD patients. This was a cross‐sectional study involving 56 ESRD patients (22 females, 34 males; mean age, 49.9 ± 14.2 years) receiving peritoneal dialysis or hemodialysis for ≥6 months in the Dialysis Unit of Necmettin Erbakan University. TAC and CAC scores were measured by using an electrocardiogram‐gated 64‐multidetector computed tomography. NLR was calculated as the ratio of the neutrophils and lymphocytes. There was a statistically significant correlation between NLR, TACS and CACS in ESRD patients (r = 0.43, P = 0.001 and r = 0.30, P = 0.02, respectively). The stepwise linear regression analysis revealed that age, as well as NLR were independent predictors of TACS. However, increased age was the only independent predictor of CACS according to linear regression analysis. Simple calculation of NLR can predict vascular calcification in ESRD patients.     

Pre‐ and Post Hemodialysis Procalcitonin Levels and Their Relationships with Immunoregulatory,Proinflammatory Cytokines in Chronic Hemodialysis Patients

Arteriosclerosis is characterized by stiffening of arteries. The incremental elastic modulus (Einc) measurement is a good marker of arterial wall stiffness. Arteriosclerosis is characterized by stiffening of arteries. Metabolic, inflammatory, and hemodynamic alterations cause structural changes and vascular complications in end‐stage renal disease. The aim of the present study was to evaluate the factors that may affect the development of arteriosclerosis by measurement of Einc in hemodialysis (HD) patients. Thirty‐two patients (16 men and 16 women) on chronic HD with a mean age of 42.2 ± 19.3 (range, 15–80) were included in the study. The carotid Einc was measured to determine arteriosclerosis by high‐resolution echo‐tracking system. Einc measurement was calculated from transcutaneous measurements of carotid arterial internal diameter and wall thickness and carotid pulse pressure. Common carotid compliance (CCC) and distensibility (CCD) were determined from changes in carotid artery diameter during systole and simultaneously measured carotid pulse pressure. Serum levels of calcium (Ca), phosphorus (P), parathormone (PTH), ferritin, C‐reactive protein (CRP), predialysis systolic blood pressure (SBP), predialysis diastolic blood pressure (DBP), pulse pressure (PP), age, HD duration, CCC, and CCD were correlated with Einc in all patients. A significant positive correlation was found between Einc and age (r = 0.40, p < 0.02), SBP (r = 0.39, p < 0.02), PP (r = 0.40, p < 0.02), Ca (r = 0.43, p < 0.01), CRP (r = 0.38, p < 0.02). As expected, Einc was correlated inversely with CCD (r = ?0.77, p < 0.0001). The correlation between Einc and HD duration, DBP, ferritin, P, PTH, and CCC was not significant. In conclusion, the stiffening of carotid artery in HD patients is related not only to hemodynamic changes (increased SBP and PP) but also to metabolic (increased Ca) and inflammatory (increased CRP) responses. Carotid Einc is an accepted independent risk factor for cardiovascular mortality. Because of the positive correlation between Einc and serum Ca, vitamin D and Ca‐containing P binder should be used carefully in HD patients.