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PubMed2003

[Vascular calcification and quality of life on diabetic dialysis patients].

The diabetic nephropathy case of our country has much NIDDM and the macroangiopathy is also merged from the time not only of the microangiopathy, compaired to the cases of chronicglomerulo-nephritis and the cases of diabetic dialysis, there is much death by ischemic heart disease, such as myocardial infarction on the latter. The quality of dialysis, such as stable dialysis, is also concerned with QOL. There are not few cases which cause the fall of blood pressure and consciousness disappearance in connection with external circulation among dialysis on diabetic dialysis patients. It is dependent on the existence of complication of ischemic cardiac disease how stable dialysis is enforced during dialysis and it gets. A vascular obstraction is related to the prognosis and QOL until it continues till a maintenance term further from an introduction of dialysis therapy. How this disease is managed makes the prognosis good.

English Abstract↗
PubMed2002

Vascular calcifications as a footprint of increased calcium load and chronic inflammation in uremic patients: a need for a neutral calcium balance during hemodialysis?

Cardiovascular complications caused by an accelerated atherosclerotic disease represent the largest single cause of mortality in chronic renal failure patients. The rapidly developing atherosclerosis of the uremic syndrome appears to be caused by a synergism of different mechanisms, such as malnutrition, oxidative stress and genetic factors. Recent studies provide evidence that chronic inflammation plays an important role in the pathogenesis of cardiovascular diseases. Hyperphosphatemia and an increased calcium-phosphate ion product have also been associated with an increased risk of death. Cardiovascular calcifications secondary to increases in phosphate and calcium load in dialysis patients might exert an important contribution to the excess cardiovascular mortality and morbidity in dialysis patients. Elevated serum levels of plasma C-reactive protein (CRP) are associated with the extent and severity of the atherosclerotic processes as well as with an increased risk of experiencing myocardial infarction and sudden cardiac death in apparently healthy subjects. In patients affected by pre-dialytic renal failure increased levels of CRP and IL-6 were recorded in 25% of our population; CRP and IL-6 were inversely related with renal function. These data suggest the activation--even in the predialytic phase of renal failure--of mechanisms known to contribute to the enhanced cardiovascular morbidity and mortality of the uremic syndrome. In recent years we have investigated the hypothesis that the chronic inflammatory state of the uremic patient could be at least in part due to the dialytic technique. We have shown that the increase of CRP in stable dialysis patients may be due to the stimulation of monocyte/macrophage by backfiltration of dialysate contaminants. During conventional dialysis, a positive calcium balance and a concomitant inflammatory state may act as cofactors in the development of cardiovascular calcifications. We suggest that this hypothesis should be verified by clinical studies. A reevaluation of the ideal calcium levels in the dialysate is warranted: a neutral intradialytic calcium balance is probably more appropriate, although not easily attainable.

Acute-Phase Reaction↗
PubMed2006

Interleukin-4 differentially regulates osteoprotegerin expression and induces calcification in vascular smooth muscle cells.

Vascular calcification is characterized by cellular transdifferentiation and expression of bone-related matrix proteins that result in the presence of bone-like structures in the vascular wall. Interleukin (IL)-4, a pleiotropic cytokine, and osteoprotegerin (OPG), an essential regulator of osteoclast biology, have both been linked to vascular disease. Here, we assessed the role of IL-4 and OPG in vascular calcification in vitro. IL-4 induced OPG mRNA levels and protein secretion by 5-fold in a dose- and time-dependent fashion in human coronary artery smooth muscle cells (CASMC). Activation of the transcription factor STAT6 preceded IL-4-induced OPG expression, and blockade of IL-4-induced STAT6 activation by the phospholipase C inhibitor D609 decreased OPG expression. Long-term exposure of IL-4 for 4 weeks resulted in transformation of CASMC towards an osteoblastic phenotype, based on the expression of the transcription factor Cbfa1 and increased mineral deposition. Notably, calcification of CASMC was inhibited by gene silencing of Cbfa1. During osteogenic transformation, IL-4 down-regulated OPG production in CASMC. IL-4 has differential effects in CASMC: While short-term exposure enhances OPG production through a STAT6-dependent mechanism, long-term exposure causes Cbfa1-dependent osteogenic transformation and a decreased production of OPG, an inhibitor of bone resorption.

Bone Resorption↗
PubMed1980

[Cardiac x-ray findings and vascular calcification in arterial obstructive disease in the pelvic and leg region. II].

In 117 patients with arterial obstructive disease in the region of pelvis and leg compared with test persons with healthy vessels the percentage of the deformation of the heart according to the classification after Richter was significantly higher for the left-side prevailing bilaterally loaded heart as well as for the left-ventricularly loaded heart. No differences could be ascertained between hypertonic and normotonic patients with ill vessels. In the patients compared with the clinically healthy test persons we registered surface-kymographically and electrokymographically more frequently a pathological marginal movement of the heart as a reference to a myocardial dysfunction. The distinct pathological surface-kymographical and electrokymographical findings on the heart correlated with the electrocardiographical findings. The data got on the heart confirmed the indication of a cardial basal therapy existing in most cases in older patients with vascular diseases. The slight diameter of the thoracic aorta as well as the restriction of the surface-kymographically provable amplitude of the movement in the region of the arc may, compared with the test persons with healthy vessels, refer to a disturbed wind kessel function of the aorta, they let us think of a primary rigidity of the wall. On the basis of the present results of examinations the sum of simply to be established X-ray findings--form of the heart, measure of the aorta, state of sclerosis, surface-kymographical findings at the heart and the aorta--may characterize an advanced vascular disease.

Angiography↗
PubMed1989

Mice carrying a CAR-2 null allele lack carbonic anhydrase II immunohistochemically and show vascular calcification.

Mutant mice reported to lack carbonic anhydrase isoenzyme II (CA II) have been examined here for immunocytochemical evidence of CA II and for histopathologic change. All histologic sites that immunostain for CA II in a wide range of organs in normal mice failed to show such immunoreactivity in the homozygous mutants. The CA II-deficient mice differed from controls in evidencing an age dependent medial calcification of small arteries in a number of organs. The male genital tract revealed the most extensive arterial calcinosis and males were possibly more affected in general than females. One or another Car-2n/Car-2n mouse showed changes additionally in uterus, small bowel, lymph nodes, or renal pelvis.

Aging↗
PubMedDate not supplied

Premature vascular calcification in a case of POEMS syndrome.

A patient with classical POEMS syndrome associated with a myeloproliferative disorder is presented, in whom extensive arterial calcification was seen at an early age in the absence of other predisposing factors. Radiographs also demonstrated several small discrete sclerotic foci elsewhere in the skeleton and areas of new bone formation around the spine which were described in previous cases. Histological studies in this patient demonstrated an osteosclerotic solitary plasmacytoma of bone and Castleman's disease of lymph nodes, both of which have previously been causally associated with POEMS syndrome. In addition, dermal infiltration by mast cells was demonstrated.

Adult↗
PubMed1990

Cutaneous vascular calcification with ulceration in hyperparathyroidism.

We report a histologically distinctive form of small blood vessel calcification that led to necrosis and ulceration of the skin. Microscopically, wedge-shaped ulcers of the skin and superficial subcutis were observed. Calcified deposits were identified in the walls of small blood vessels at the ulcer bases. Recanalized thrombi occluded the lumina of some of the calcified vessels. On the basis of these distinctive histologic findings, hyperparathyroidism was accurately predicted. These changes have previously been cited in the internal medicine and dermatology literature but, to our knowledge, not in the pathology literature. We believe that these lesions are not rare and are probably often overlooked by pathologists. The histologic and clinical findings in two cases are presented.

Adult↗
PubMed2005

[Bone mineral density and vascular calcification].

It is of interest that in the general population, low bone mass is associated with a higher mortality rate due to atherosclerotic cardiovascular disease. In addition, the degree of aortic calcification is closely related with a lower bone mineral density (BMD). These results suggest that a low BMD may predict increased arterial stiffness. In ESRD patients, advanced arterial stiffness and low BMD due to renal osteodystrophy are not uncommon. Moreover, the initiation and progression of arterial stiffness and bone loss are accelerated by the same factors such as hyperphosphatemia secondary to chronic renal failure. A lower BMD might be more clearly associated with a higher PWV in dialysis patients than in the general population. To prove this hypothesis, we performed a preliminary cross-sectional study to investigate the relationship between BMD, as determined by calcaneal osteo-sono index (OSI), and arterial stiffness, as measured by the brachial-ankle PWV (baPWV). Our study demonstrated that calcaneal OSI, a marker for estimated BMD, has a powerful predictor of arterial stiffness, independent of classic risk factors, malnutrition, or inflammation markers. The evaluation of BMD needs to grasp not only the status of bone disease, but also the degree of arterial stiffness.

Bone Density↗
PubMed2005

Vascular calcification in patients with renal failure: culprit or innocent bystander?

The mortality from cardiovascular events in CKD and dialysis patients is substantially higher than in the general population. VC is ubiquitous and progresses rapidly in this patient population. Although there has been progress in the understanding of the pathogenesis and correlates of VC, much work needs to be done in this area. The role of calcium and, probably, phosphate (obligatory participants) is unquestionable, but the understanding of the paracrine and molecular determinants of VC in renal failure is continuously evolving. VC is probably a dynamic process resulting from the imbalance between molecules that promote and those that inhibit VC. The understanding of latter area has recently evolved with identification of new signaling pathways with molecules such as osteoprotegerin, fetuin-A, and MPG. From a clinical perspective, new modalities such as EBCT and MDCT allow noninvasive detection and quantification of VC. VC may represent a potential useful index for prognostic stratification and treatment planning in patients who have renal failure. At present, however, the data on the prognostic value of VC are available only in populations of patients who have normal renal function. Large-scale, prospective, observational studies should be designed to identify the determinants of VC and to define the prognostic role of calcium scoring in cohorts of patients who have predialysis CKD and with ESRD.

Atherosclerosis↗
PubMed2000

Phosphate regulation of vascular smooth muscle cell calcification.

Vascular calcification is a common finding in atherosclerosis and a serious problem in diabetic and uremic patients. Because of the correlation of hyperphosphatemia and vascular calcification, the ability of extracellular inorganic phosphate levels to regulate human aortic smooth muscle cell (HSMC) culture mineralization in vitro was examined. HSMCs cultured in media containing normal physiological levels of inorganic phosphate (1.4 mmol/L) did not mineralize. In contrast, HSMCs cultured in media containing phosphate levels comparable to those seen in hyperphosphatemic individuals (>1.4 mmol/L) showed dose-dependent increases in mineral deposition. Mechanistic studies revealed that elevated phosphate treatment of HSMCs also enhanced the expression of the osteoblastic differentiation markers osteocalcin and Cbfa-1. The effects of elevated phosphate on HSMCs were mediated by a sodium-dependent phosphate cotransporter (NPC), as indicated by the ability of the specific NPC inhibitor phosphonoformic acid, to dose dependently inhibit phosphate-induced calcium deposition as well as osteocalcin and Cbfa-1 gene expression. With the use of polymerase chain reaction and Northern blot analyses, the NPC in HSMCs was identified as Pit-1 (Glvr-1), a member of the novel type III NPCs. These data suggest that elevated phosphate may directly stimulate HSMCs to undergo phenotypic changes that predispose to calcification and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions. The full text of this article is available at http://www.circresaha.org.

Arteries↗
PubMed1976

Calciphylaxis in man. A syndrome of tissue necrosis and vascular calcification in 11 patients with chronic renal failure.

Eleven patients with chronic renal failure and presumed secondary hyperparathyroidism developed a syndrome of medial calcinosis of the arteries and painful ischemic ulcers of the fingers, legs, or thighs, or any combination of the three. Five patients required maintenance hemodialysis; six had functioning renal homografts. Severe hyperphosphatemia had existed in each; seven showed roentgenographic evidence of subperiosteal resorption. Similarities are evident between the lesions and experimentally produced calciphylaxix. The lesions demonstrated a relentless, progressive course, with serious morbidity and mortality. Hyperplastic or adenomatours parathyroid tissue was removed from ten of 11 patients unergoing surgical procedures; healing followed in seven patients. Treatment with phosphate-binding antacids to lower serum phosphorus levels may prevent this syndrome. Total or subtotal parathyroidectomy should be considered when ischemic skin lesions appear in uremic patients or in renal transplant recipients.

Adolescent↗