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PubMed2005

Vascular ossification-calcification in metabolic syndrome, type 2 diabetes mellitus, chronic kidney disease, and calciphylaxis-calcific uremic arteriolopathy: the emerging role of sodium thiosulfate.

BACKGROUND: Vascular calcification is associated with metabolic syndrome, diabetes, hypertension, atherosclerosis, chronic kidney disease, and end stage renal disease. Each of the above contributes to an accelerated and premature demise primarily due to cardiovascular disease. The above conditions are associated with multiple metabolic toxicities resulting in an increase in reactive oxygen species to the arterial vessel wall, which results in a response to injury wound healing (remodeling). The endothelium seems to be at the very center of these disease processes, acting as the first line of defense against these multiple metabolic toxicities and the first to encounter their damaging effects to the arterial vessel wall. RESULTS: The pathobiomolecular mechanisms of vascular calcification are presented in order to provide the clinician-researcher a database of knowledge to assist in the clinical management of these high-risk patients and examine newer therapies. Calciphylaxis is associated with medial arteriolar vascular calcification and results in ischemic subcutaneous necrosis with vulnerable skin ulcerations and high mortality. Recently, this clinical syndrome (once thought to be rare) is presenting with increasing frequency. Consequently, newer therapeutic modalities need to be explored. Intravenous sodium thiosulfate is currently used as an antidote for the treatment of cyanide poisoning and prevention of toxicities of cisplatin cancer therapies. It is used as a food and medicinal preservative and topically used as an antifungal medication. CONCLUSION: A discussion of sodium thiosulfate's dual role as a potent antioxidant and chelator of calcium is presented in order to better understand its role as an emerging novel therapy for the clinical syndrome of calciphylaxis and its complications.

Animals↗
PubMed2001

Non-invasive assessments of cardiovascular disease in patients with renal failure.

Vascular calcification is common in patients with chronic renal failure, and it may contribute to the very high mortality rate from cardiovascular causes in the end-stage renal disease population. Vascular calcification in chronic renal failure can arise from the calcification of the intimal layer of arteries as a result of atherosclerosis or from medial wall calcification due largely to alterations in mineral metabolism. Although several reports indicate that coronary artery calcification, as measured by electron-beam computed tomography, is quite common in patients with end-stage renal disease who are treated with dialysis, the clinical significance of these findings remain uncertain. In the general population, electron-beam computed tomography evidence of coronary calcification serves as a useful index of atherosclerotic burden and has value as a predictor of adverse coronary events. The relationship between coronary artery calcification and atherosclerotic cardiovascular disease has not been adequately studied, however, in patients with end-stage renal disease, and calcification scores in this population may reflect both intimal and medial wall calcification. Assessments using coronary angiography are needed to determine the diagnostic value of electron-beam computed tomography as a predictor of atherosclerotic cardiovascular disease in patients with chronic renal failure. Nevertheless, electron-beam computed tomography makes it possible to detect the presence and monitor the progression of coronary calcification in those undergoing long-term dialysis. The technique may provide important information about the impact of new therapeutic strategies aimed at reducing the risks of vascular calcification in those with chronic renal failure.

Cardiovascular Diseases↗
PubMed2003

Association of low fetuin-A (AHSG) concentrations in serum with cardiovascular mortality in patients on dialysis: a cross-sectional study.

BACKGROUND: Vascular calcification is the most prominent underlying pathological finding in patients with uraemia, and is a predictor of mortality in this population. Fetuin-A (alpha2-Heremans Schmid glycoprotein; AHSG) is an important circulating inhibitor of calcification in vivo, and is downregulated during the acute-phase response. We aimed to investigate the hypothesis that AHSG deficiency is directly related to uraemic vascular calcification. METHODS: We did a cross-sectional study in 312 stable patients on haemodialysis to analyse the inter-relation of AHSG and C-reactive protein (CRP) and their predictive effect on all-cause and cardiovascular mortality, over a period of 32 months. Subsequently, we tested the capacity of serum to inhibit CaxPO4 precipitation in patients on long-term dialysis (n=17) with apparent soft-tissue calcifications, and in those on short-term dialysis (n=8) without evidence of calcifications and cardiovascular disease. FINDINGS: AHSG concentrations in serum were significantly lower in patients on haemodialysis (mean 0.66 g/L [SD 0.28]) than in healthy controls (0.72 [0.19]). Low concentrations of the glycoprotein were associated with raised amounts of CRP and with enhanced cardiovascular (p=0.031) and all-cause mortality (p=0.0013). Sera from patients on long-term dialysis with low AHSG concentrations showed impaired ex-vivo capacity to inhibit CaxPO4 precipitation (mean IC50: 9.0 microL serum [SD 3.1] vs 7.5 [0.8] in short-term patients and 6.4 [2.6] in controls). Reconstitution of sera with purified AHSG returned this impairment to normal. Interpretation AHSG deficiency is associated with inflammation and links vascular calcification to mortality in patients on dialysis. Activated acute-phase response and AHSG deficiency might account for accelerated atherosclerosis in uraemia.

Blood Proteins↗
PubMed2000

Mechanism of atherosclerotic calcification.

Calcification is almost invariably associated with atherosclerotic plaque lesions. Recent data suggest that plaque calcification is an active, regulated process similar to osteogenesis. In order to clarify the mechanism of plaque calcification, we developed an in vitro model of vascular calcification by utilizing bovine vascular smooth muscle cells (BVSMCs). This model is useful in that diffuse and massive calcification can be induced within 2 weeks and thereby biochemical analyses of vascular calcification can be performed. We have analyzed several aspects of vascular calcification by using this model and demonstrated as follows: 1) in vitro calcification of BVSMCs is regulated by calciotropic hormones and BVSMCs are equipped with a unique autocrine and/or paracrine system regulating calcium metabolism. 2) Sodium-dependent phosphate cotransport plays a crucial role in BVSMC calcification as well as in mineralization of skeletal tissues. 3) BVSMCs acquire osteoblastic phenotype under certain conditions. Finally, we discuss the roles of macrophages in the development of atherosclerotic calcification. Interferon-gamma (IFN-gamma) induces gene expression of 25-hydrovitamin D-1 alpha-hydroxylase (1 alpha OHase) and its activity in macrophages. Since 1 alpha OHase can locally convert 25-hydroxyvitamin D into 1 alpha, 25-dihydroxyvitamin D (1,25(OH)2D), an active metabolite of vitamin D, it is suggested that local production of 1,25(OH)2D by macrophages may promote atherosclerotic calcification. Moreover, macrophages may be involved in the phenotypic changes of vascular smooth muscle cells (VSMCs) to acquire calcifying capacity. Therefore, the phenotypic changes of VSMCs in atherosclerotic plaque may contribute to the development of atherosclerotic calcification.

Animals↗
PubMed2001

Bone loss and the progression of abdominal aortic calcification over a 25 year period: the Framingham Heart Study.

Vascular calcification and osteoporosis are common age-related processes that are prominently displayed on routine lateral lumbar spine radiographs as dense calcium mineral deposits of the aorta that lie adjacent to osteopenic vertebrae. Using a population-based cohort of older men and women, we tested the hypothesis that the progression of vascular calcification of the abdominal aorta should be greatest in those individuals with the greatest amount of bone loss. From the original population-based Framingham Heart Study cohort, 364 women and 190 men had lateral lumbar spine and hand radiographs performed between 1966 and 1970 and repeated between 1992 and 1993. The lateral lumbar films were read for the presence of aortic calcification using a semiquantitative method, and the hand films were read for second metacarpal relative cortical area (MCA). Using multivariate regression techniques, the 25-year progression of the abdominal aortic calcification index was examined in relation to the change in the MCA, while adjusting for recognized risk factors for atherosclerotic cardiovascular disease. During the 25 years of follow-up, the MCA decreased by 22.4% in women (from 79.6 +/- 7.8 (SD) to 61.8 +/- 10.3) and by 13.3% in men (from 80.6 +/- 6.9 to 69.9 +/- 8.3). The aortic calcification score increased over eightfold in women (from 1.2 +/- 2.7 (SD) to 9.9 +/- 6.7) and sixfold in men (from 1.6 +/- 2.8 to 9.6 +/- 6.3). There was a significant association between percent change in MCA and change in aortic calcification index (P = 0.01) in women after controlling for all potential confounders. No association was observed in men (P = 0.50), including the 50% of men with the greatest bone loss. This is the first longitudinal study to show that women with the greatest magnitude of bone loss also demonstrate the most severe progression of abdominal aortic calcification, suggesting that the two processes may be related.

Absorptiometry, Photon↗
PubMedDate not supplied

Gene polymorphism association studies in dialysis: the nutrition-inflammation axis.

Although traditional risk factors for cardiovascular disease are common in dialysis patients, they alone cannot explain the unacceptably high prevalence of vascular disease in this patient group. Much recent interest has therefore focused on the role of various nontraditional cardiovascular risk factors, such as inflammation, wasting, obesity, vascular calcification, and oxidative stress. In addition, genetic factors such as single nucleotide polymorphisms (SNPs) may significantly influence the immune response, the levels of inflammatory markers and body composition, as well as the prevalence of vascular calcification in this patient group. While genetic variations in the tumor necrosis factor (TNF)-alpha-308 and interleukin (IL)-10 -1082 SNPs seem to be consistently associated with adverse clinical outcome in end-stage renal disease (ESRD) patients, the results regarding genetic variations in the IL-6 gene have been conflicting. To elucidate the respective role of DNA polymorphisms in the IL-6 and C-reactive protein (CRP) genes, as well as genes that encode vascular calcification inhibitors (such as fetuin-A, matrix Gla protein, and osteoprotegerin), sufficiently powered studies are needed in which both the protein product and the specific phenotype are determined. In addition, polymorphisms in genes related to body composition may be excellent candidates for analysis in the ESRD population, since nutritional parameters are strongly associated with adverse events in these patients. It seems conceivable that in the future, prognostic or predictive multigene DNA assays (which allow a simultaneous and rapid assessment of multiple genetic variants) will provide nephrologists with a more precise approach for the identification of "high-risk" ESRD patients and the development of accurate individualized treatment strategies.

Biomarkers↗
PubMed2006

Optical imaging of hydroxyapatite in the calcified vasculature of transgenic animals.

OBJECTIVE: To detect the hydroxyapatite component of vascular calcification in vivo so that the process of calcium deposition can be studied in transgenic model systems. METHODS AND RESULTS: We have previously developed a near-infrared fluorescent bisphosphonate derivative that binds with high affinity and specificity to hydroxyapatite, and an intraoperative near-infrared fluorescence imaging system for small animals. Using these tools, and a transgenic mouse strain with homozygous deletion of the matrix GLA protein (Mgp(-/-)), we demonstrate that the hydroxyapatite component of vascular calcification can be detected in vivo with high sensitivity, specificity, and resolution. CONCLUSIONS: The hydroxyapatite component of vascular calcification can be detected optically, in real-time, without sacrifice of the animal. It is now possible to study the earliest events associated with vascular mineralization, at the cell and organ level, and to monitor the process in living animals.

Animals↗
PubMed1997

Impact of spinal degenerative changes on the evaluation of bone mineral density with dual energy X-ray absorptiometry (DXA).

The purpose of this study is to evaluate degenerative factors in a postmenopausal patient group and differentiate the influence on bone mineral density (BMD) measurements by dual-energy X-ray absorptiometry (DXA). The patients and methods included an investigation of 144 postmenopausal women (mean 63.3 years) with PA-DXA of the spine. Degenerative factors (osteophytes, osteochondrosis, scoliosis, and vascular calcification) were evaluated from plain lumbar radiographs, their estimated probability was analyzed as a function of age, and their influence on BMD measured by PA-DXA was determined. The results of the study revealed osteophytes in 45.8%, vascular calcifications in 24.3%, scoliosis in 22.2%, osteochondrosis in 21.5%. The estimated probability for degenerative factors increased from 35 to 80% in the 55- to 70- year age group. Osteophytes and osteochondrosis were associated with up to a 14% increase in BMD values (P < 0.001). Vascular calcifications showed a positive trend, whereas scoliosis did not show a discernible influence.We concluded that degenerative factors, except for scoliosis, showed an influence on BMD as measured by DXA. Their prevalence increased rapidly between 55 and 70 years of age. Interpretation of PA-DXA spine data for subjects of or above this age range should be complemented by plain film radiographs.

Absorptiometry, Photon↗
PubMed2002

[Genes involved in the relationship between bone and blood vessel MGP, klotho, OPG].

Recent gene deletion experiments in mice have provided important insights into the molecular mechanisms of vascular calcification. Mice lacking Mgp, klotho, and Opg developed diffuse arterial calcification. These findings favor the hypothesis that vascular calcification appears spontaneously in the absence of an inhibitory protein.

English Abstract↗
PubMed2004

Vascular biology in uremia: insights into novel mechanisms of vascular injury.

Cardiovascular disease is the leading cause of death in patients with end-stage renal disease. Although the prevalence of traditional atherosclerotic risk factors is increased in patients with chronic kidney disease, these traditional risk factors alone do not seem to account for the increased cardiovascular mortality. It has been proposed that additional risk factors may play a role in vascular injury. Among nontraditional risk factors, chronic inflammation, oxidative stress, and vascular calcification have been implicated in the accelerated athersclerosis of chronic kidney disease. Uremia is a proinflammatory state. Elevated levels of the proinflammatory cytokine interleukin-6 and suppressed levels of the anti-inflammatory cytokine interleukin-10 are present in chronic kidney disease and have been implicated in accelerated atherosclerosis. Uremia also results in increased oxidative stress. Asymmetric dimethyl arginine and myeloperoxidase may be critical mediators of the endothelial damage that results from oxidative stress. Finally, the uremic milieu seems to promote vascular calcification. The abundance of proinflammatory cytokines, the possible deficiency in calcification inhibitory proteins and the high phosphorus that are often present in uremia contribute to vascular calcification. Smooth muscle cells in calcifying lesions undergo phenotypic changes and molecular reprogramming that are reminiscent of endochondral bone formation during embryogenesis.

Calcinosis↗
PubMed1974

Effects of age, sex, and polycystic disease on progressive bone disease of renal failure.

A study of 150 patients undergoing haemodialysis has shown that age had a striking effect on the radiological presentation of renal bone disease, erosions being common in the young and uncommon in older patients and vascular calcification showing opposite trends to this. Men aged 20 to 59 years had a greater tendency to develop erosions than did women in this age range. Examination of a group of 53 patients over a period of five years showed that the half time for the development of vascular calcification was 4.6 years, erosions 26.7 years, and fractures 6.9 years. Nine out of 16 polycystic patients matched for age and sex with 50 controls did not develop erosions and had consistently less vascular calcification than the controls when examined over a six-year period.

Adolescent↗
PubMed2005

Low fetuin-A levels are associated with cardiovascular death: Impact of variations in the gene encoding fetuin.

BACKGROUND: Vascular calcification is common among end-stage renal disease (ESRD) patients and a central characteristic of the atherosclerotic cardiovascular disease observed in dialysis patients. Fetuin-A, a circulating calcium-regulatory glycoprotein that inhibits vascular calcification, is associated with inflammation and outcome in dialysis patients. In the present study, we evaluated the association between fetuin-A, clinical phenotype, and outcome, as well as the impact of fetuin gene (AHSG) polymorphisms on the protein product and outcome. METHODS: In a cohort of 258 (161 males) ESRD patients starting renal replacement therapy [glomerular filtration rate (GFR) 6.8 +/- 0.2 mL/min] aged 52 +/- 1 years the following parameters were studied: presence of malnutrition (subjective global assessment), comorbidity [diabetes mellitus and clinical manifest cardiovascular disease (CVD)], carotid plaques (N= 101), hs-CRP, fetuin-A, S-albumin, interleukin (IL)-6, and single nucleotide polymorphisms (SNPs) in the AHSG gene (N= 215) at amino acid positions Thr248Met (C-->T), Thr256Ser (C-->G), Asp276Asn (G-->A), and Arg317Cys (C-->T). RESULTS: Both all-cause (P < 0.001) and cardiovascular (P < 0.001) mortality were associated with low fetuin-A levels independently of age, smoking, diabetes, S-albumin, CVD, and inflammation (CRP > or =10 mg/L). Inflamed (0.199 vs. 0.247 g/L; P < 0.01) and malnourished (0.207 vs. 0.262 g/L; P < 0.05) patients had significantly lower median fetuin-A than noninflamed and well-nourished ESRD patients, respectively. In a logistic regression model (N= 101), fetuin-A was significantly (P < 0.05) associated with the presence of carotid plaques independently of age, CVD, diabetes, S-albumin, gender, and inflammation. Significant correlations were observed between fetuin-A and both S-albumin (Rho = 0.30; P < 0.0001) and IL-6 (Rho =-0.21; P < 0.01). Patients with the AHSG 256Ser allele had lower serum fetuin-A levels, and higher all-cause and cardiovascular mortality rate if they were inflamed. CONCLUSION: The present study shows that a low fetuin-A level is associated with malnutrition, inflammation, and atherosclerosis (carotid plaques), as well as with increased cardiovascular and all-cause mortality. Because the present study demonstrates an effect of variations in the AHSG gene on both circulating fetuin-A levels and outcome, this indicates that ESRD patients with the AHSG 256Ser allele are at risk of accelerated vascular calcification.

Blood Proteins↗
PubMed2003

Medical management of secondary hyperparathyroidism in chronic renal failure.

Abnormalities in calcium and phosphorus metabolism are common, and metabolic bone disease develops often in patients with chronic renal failure (CRF). Effective clinical management includes measures to control phosphorus retention and prevent hyperphosphataemia, to maintain serum calcium concentrations within the normal range and to prevent excess parathyroid hormone (PTH) secretion by the judicious use of vitamin D sterols. Certain of these interventions appear to increase the risk of soft tissue and vascular calcification in patients with end-stage renal disease (ESRD), changes that may contribute to the development of cardiovascular disease. Current therapeutic approaches are thus being re-evaluated in an effort to limit these risks. Despite the importance of controlling phosphorus retention and preventing hyperphosphataemia in patients with CRF, current management strategies often are inadequate, particularly in those ingesting diets containing adequate amounts of protein. Results from clinical trials using daily haemodialysis strongly suggest that thrice-weekly haemodialysis regimens are only marginally adequate for achieving weekly phosphorus balance in many patients with ESRD. The safety of large oral doses of calcium as a phosphate-binding agent in patients with ESRD has also been questioned because excess amounts of calcium that are absorbed from the gastrointestinal tract may lead to ongoing calcium retention in those with little or no residual renal function. Arterial calcification and cardiac valve calcification are two serious complications that adversely affect cardiovascular haemodynamics. The use of large, often supraphysiological, doses of calcitriol or other vitamin D sterols to treat secondary hyperparathyroidism may aggravate hypercalcaemia and hyperphosphataemia, further increasing the risk of soft tissue and vascular calcification. Phosphate-binding agents that do not contain calcium, new vitamin D analogues and calcimimetic compounds offer new therapeutic alternatives for managing renal osteodystrophy. The integration of these novel agents into existing treatment regimens may provide safer and more effective methods for controlling secondary hyperparathyroidism and renal bone disease, while limiting the risks of soft tissue and vascular calcification in patients with CRF.

Administration, Oral↗
PubMed2005

Myocardial stiffness, cardiac remodeling, and diastolic dysfunction in calcification-prone fetuin-A-deficient mice.

Accelerated atherosclerosis in dialysis patients is characterized by severe vascular calcification, and the magnitude of vascular calcification is associated with increased cardiovascular mortality. Calcification-dependent arterial stiffness is considered to be a major determinant of cardiac failure in uremia. Fetuin-A/alpha(2)-Heremans-Schmid glycoprotein is an abundant serum protein with powerful calcification inhibitory properties. Fetuin-A deficiency was recently linked to cardiovascular mortality in dialysis patients. Fetuin-A knockout (fetuin-KO) mice spontaneously develop widespread soft tissue calcification, including significant myocardial calcification, whereas larger arteries are spared. Therefore, this investigation offers the unique opportunity to study the functional role of isolated myocardial calcification independent of arterial stiffness by assessing the hemodynamics of fetuin-KO mice. Cardiac output in fetuin-KO mice was lower than in wild-type mice (fetuin-KO 1.81 +/- 0.18 versus WT 2.45 +/- 0.29 ml/min per g; P < 0.005), and fetuin-KO mice were refractory to dobutamine stimulation. Left ventricular relaxation was significantly impaired in fetuin-KO hearts with the relaxation index reduced by 23% (P < 0.005). After ischemia, fetuin-KO hearts displayed a continuous decline in left ventricular developed pressure after the initial phase of reperfusion, resulting in 77 +/- 15% of preischemic left ventricular developed pressure (P < 0.05 versus wild-type). In fetuin-KO mice, dystrophic cardiac calcification, with myocardial calcium contents increased 60-fold, was associated with profound induction of profibrotic TGF-beta and downstream collagen and fibronectin mRNA synthesis. In conclusion, independent of arterial stiffness, calcification-associated "myocardial stiffness" characterized by cardiac fibrosis, diastolic dysfunction, impaired tolerance to ischemia, and catecholamine resistance thus may constitute an underestimated cardiovascular risk factor that contributes to cardiac failure in calcification-prone states.

Animals↗
PubMed2001

[48-year old woman with diffuse pulmonary calcifications after allogeneic kidney transplantation. A rare manifestation of tertiary hyperparathyroidism].

HISTORY: A 48-year-old woman was hospitalized because of the presence of asymptomatic bilateral pulmonary infiltrates in the conventional chest radiograph. An antibiotic treatment administered 3 months before had been without any effect on the radiological aspect. The patient had had an end-stage renal disease of unknown cause and was on hemodialysis since 1993. 1997 she received a cadaveric renal transplant. INVESTIGATIONS: Computed tomography scan detected the infiltrates as diffuse calcifications mainly at the lung bases. Extended arterial vascular calcifications were also found. Since approximately 4 years calcium-phosphorus product and parathyroid hormone had been increased. TREATMENT AND COURSE: Because of the long-term increased calcium-phosphorus product and the high parathyroid hormone levels we interpreted the pulmonary calcifications as a result of the tertiary hyperparathyroidism. After parathyroidectomy calcium-phosphorus product and PTH levels normalized, but our patient suffered from increasing disturbances of the peripheral blood circulation induced by the vascular calcifications, necessitating amputation of finger and toe tips. CONCLUSION: Patients with renal failure should undergo regular controls of calcium, phosphorus and parathyroid hormone when creatinine clearance is below 50 ml/min/1.73 m2. Only an early medical treatment can prevent the various complications induced by the secondary or tertiary hyperparathyroidism. If medical therapy fails, parathyroidectomy has to be done. Especially before renal transplantation the extent of hyperparathyroidism has to be carefully analyzed and treated aggressively, if necessary by surgery before the date of transplantation.

Calcinosis↗
PubMed1997

Arterial calcification in face of osteoporosis in ageing: can we blame oxidized lipids?

Although vascular calcification is present in the vast majority of those aged over 70 years and causes serious cardiovascular dysfunction, strategies for its prevention and effective management are currently not available because the mechanism of its pathogenesis is unknown. Recently, similarities between mineralization in the vessel wall and in bone have been recognized. In this review, current understanding of the mechanisms involved in atherosclerotic calcification is summarized. In addition, several observations that may explain the paradox of vascular calcification in the face of osteoporosis are noted, emphasizing the possible role of lipid oxidation products.

Aging↗
PubMed2005

Osteopontin expression and adventitial angiogenesis induced by local vascular endothelial growth factor 165 reduces experimental aortic calcification.

BACKGROUND: Vascular calcification is a common pathologic and precisely regulated process involving bone-associated proteins such as osteopontin. In this study, we investigated mechanisms by which recombinant human vascular endothelial growth factor 165 protects the arterial wall from severe vascular remodeling, including calcification, a newly discovered biologic action of vascular endothelial growth factor. METHODS: In a rabbit model of thoracic aortic end-to-end anastomosis that simulates cardiovascular intervention, recombinant human vascular endothelial growth factor 165 at a dose of 0.75 mug (n = 19) or albumin (control; n = 19) was delivered intraluminally and on the serosal surface. Animals were killed, and aortic tissue was evaluated by Western blotting, immunohistochemistry, and immunofluorescence at 4, 8, and 24 hours; 1 week; and 1 month after surgery. RESULTS: All controls revealed extensive aortic medial calcification at 1 month, whereas calcification was significantly reduced or absent with vascular endothelial growth factor treatment. Compared with controls, vascular endothelial growth factor treatment resulted in an earlier infiltration of macrophages in the vessel media (at 8 hours: 5.7 +/- 2.3 macrophages per high-power field in control vs 32.1 +/- 7.5 in vascular endothelial growth factor-treated aortas; P < .001), whereas controls showed an increase in macrophages starting at 1 week (24.1 +/- 6.9 vs 4.3 +/- 1.8; P < .001). Osteopontin expression was transiently increased and detected in macrophages and endothelial cells in vascular endothelial growth factor-treated vessels, and adventitial microvascular density was significantly increased by 1 week (9.5 +/- 0.43 vs 25.0 +/- 1.3; P < .001). CONCLUSIONS: Our data suggest that exogenous vascular endothelial growth factor is capable of increasing adventitial angiogenesis and shifting macrophage infiltration and osteopontin expression in the media to an earlier time point, thereby promoting prompt repair and diminishing vascular remodeling and calcification after acute vascular injury.

Animals↗
PubMed2006

Left ventricular hypertrophy: is hyperphosphatemia among dialysis patients a risk factor?

Cardiovascular disease occurs in ESRD patients at rates that are far higher than is seen in the general population, and cardiovascular deaths account for the majority of deaths among dialysis patients. Abnormal mineral metabolism is a novel cardiovascular risk factor among dialysis patients. Recently published results demonstrated that even with good control of BP and anemia, conventional hemodialysis is associated with significant left ventricular hypertrophy (LVH); however, daily hemodialysis was associated with a significant reduction in LV mass index (LVMI). Furthermore, it was shown that control of serum phosphorus correlates with the reduction in LVMI. These data suggest a novel mechanism for the deleterious effect of elevated serum phosphorus on cardiovascular outcomes among hemodialysis patients: LVH. Other investigators have noted an association of hyperphosphatemia and LVH; however, this study was the first to demonstrate that improvement in serum phosphorus is associated with reduction in LVM. In addition, it is shown that daily hemodialysis is an effective modality in improving serum phosphorus through significantly improved phosphorus removal. Elevated serum phosphorus leads to vascular calcification, which can lead to LVH by decreasing vascular compliance. However, our study showed an improvement in LVMI during a 12-mo period. Because vascular calcification is unlikely to remit over this time period, it is proposed that serum phosphorus has a reversible, cardiotoxic effect that leads to LVH that can be reversed successfully with good control of serum phosphorus.

Humans↗