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PubMed2003

Cinacalcet: AMG 073, Calcimimetics--Amgen/NPS Pharmaceuticals, KRN 1493, NPS 1493.

Cinacalcet [AMG 073, KRN 1493, NPS 1493] is an orally active, second-generation calcimimetic compound licensed by NPS Pharmaceuticals to Amgen in the US for potential treatment of hyperparathyroidism (HPT). Cinacalcet modulates (increases the sensitivity of) calcium receptors on the surface of parathyroid cells thereby inhibiting the oversecretion of parathyroid hormone, which characterises HPT. It also represents a potentially significant advance for chronic kidney disease patients diagnosed with secondary HPT, a common yet serious metabolic disorder where parathyroid hormone levels are elevated. Patients with this disease can suffer from bone disease, bone pain and fractures, soft tissue calcification, vascular calcification and cardiovascular complications. Amgen has rights to develop and sell cinacalcet throughout the world except in Japan, Taiwan and China, where the compound was licensed to Kirin Brewery. Kirin is developing it as KRN 1493 in phase II clinical studies in Japan. In December 2001, commencement of a phase III clinical trial with cinacalcet for the treatment of secondary HPT, triggered a 3 million US dollars milestone payment to NPS Pharmaceuticals. In September 2003, submission of an NDA to the US FDA for cinacalcet for secondary HPT will be followed by a milestone payment of 6 million US dollars to NPS. NPS, Kirin and Amgen were also developing another compound, tecalcet, for HPT, but that project has been discontinued in favour of cinacalcet. In September 2003, Amgen submitted an NDA to the US FDA for secondary HPT in patients with chronic kidney disease. In April 2003, Amgen announced positive results from a phase III clinical trial with cinacalcet in patients with secondary HPT. In a clinical study in patients on dialysis suffering from the effects of chronically elevated levels parathyroid hormone, cinacalcet appeared to be safe and well tolerated and was significantly more effective than placebo. Two more additional efficacy studies with cinacalcet have also been completed. Phase II trials of cinacalcet in dialysis patients with secondary HPT and in patients with primary HPT were successfully completed.

Chronic Disease↗
PubMed2004

Taurine prevents beta-glycerophosphate-induced calcification in cultured rat vascular smooth muscle cells.

Vascular calcification is an ectopic calcification that commonly occurs in atherosclerosis. Because taurine was previously shown to protect against cardiovascular diseases, the effect of taurine on vascular calcification was evaluated in calcified vascular smooth muscle cells (VSMCs) of rat in vitro in the present study. Osteoblastic differentiation, calcification, and proliferation in VSMCs were detected in the presence and absence of taurine. Alkaline phosphatase (ALP), cellular calcium content, and (45)Ca accumulation were measured as the indicators of osteoblastic differentiation and calcification. Incubation of VSMCs with Beta-glycerophosphate for 10 days induced an osteoblast-like morphological change. The activity of ALP was enhanced. Calcium content and (45)Ca uptake were increased in these cells. Calcification of these VSMCs was demonstrated with Beta-glycerophosphate treatment. In association with these alterations, cell proliferation, detected by cell counting, [(3)H]thymidine ([(3)H]TdR), and [(3)H]leucine ([(3)H]Leu) incorporation, was also increased in these calcified VSMCs. Taurine at 20 mmol/l decreased calcium content, (45)Ca(2+) uptake, and ALP activity both after early and late treatment, in which a reduction of the cell count, [(3)H"]TdR, and [(3)H]Leu incorporation of calcified VSMCs was also noted. Compared with the calcified group, morphological changes in the VSMCs of the early-treated group were deferred. These results demonstrated that calcification of VSMCs could be alleviated by taurine. Taurine treatment appeared to be more beneficial when the treatment was started earlier.

Animals↗
PubMed2003

Effects of adrenomedullin, C-type natriuretic peptide, and parathyroid hormone-related peptide on calcification in cultured rat vascular smooth muscle cells.

To clarify the regulating mechanism of vascular calcification, the investigators observed the effects of three vasoactive peptides, adrenomedullin (ADM), C-type natriuretic peptide (CNP), and parathyroid hormone-related peptide (PTHrP) on calcification in rat vascular smooth muscle cells (VSMCs). Beta-glycerophosphate stimulated growth and calcification in VSMCs. Adrenomedullin and CNP lowered beta-glycerophosphate-induced increase in VSMC growth. All three vasoactive peptides attenuated the increases of 45Ca accumulation, calcium content, and alkaline phosphatase activity in calcified VSMCs. As for comparing the inhibitory effects, the strongest was PTHrP. Both ADM and PTHrP increased cyclic adenosine monophosphate (cAMP) content in calcified VSMCs, but CNP upregulated cyclic guanosine monophosphate (cGMP) content. The PKA inhibitor PKAI completely reversed the inhibition of ADM on cell growth and all inhibitory effects of PTHrP on the parameters of calcification. The PKG inhibitor H8, however, strongly antagonized all the inhibitory effects of CNP on calcification. These data suggested that beta-glycerophosphate-induced calcification in VSMCs was inhibited by ADM, CNP, and PTHrP. Adrenomedullin and PTHrP inhibited VSMC calcification partially through the cAMP/PKA pathway, whereas CNP inhibited VSMC calcification through the cGMP/PKG pathway. This study could be of help in understanding the pathogenesis of vascular calcification, and providing new target for clinical treatment of cardiovascular diseases associated with vascular calcification.

Adrenomedullin↗
PubMed2002

[Ectopic calcification in dialysis patients].

Vascular calcification is the most important type of the ectopic calcinosis in dialysis patients. Hyperphosphatemia is an independent risk factor for the vascular calcification. A sodium-dependent phosphate co-transporter is associated with an increase in the intracellular phosphate concentration in vascular cells. After degeneration and/or apoptosis of smooth muscle cells in the vascular walls, macrophage infiltration into the calcified tissues followed by production of bone matrix protein leads to the vascular calcification. Uremic conditions such as hyperphosphatemia may enhance the vascular calcification. Therefore, we should treat the vascular calcification in association with bone remodeling in dialysis patients.

English Abstract↗
PubMed2005

Smooth muscle cells deficient in osteopontin have enhanced susceptibility to calcification in vitro.

OBJECTIVE: Vascular calcification is an actively regulated process, correlating with cardiovascular morbidity and mortality especially in patients with diabetes and chronic renal diseases. Osteopontin (OPN) is abundantly expressed in human calcified arteries and inhibits vascular calcification in vitro and in vivo. How OPN functions in vascular calcification, however, is less clear. METHODS: Smooth muscle cells (SMCs) were isolated from aortas of OPN knock-out (OPN-/-) and wild type (OPN+/+) mice. RESULTS: OPN-/- SMCs were identical to OPN+/+ SMCs in morphology and stained positively for SM lineage proteins, desmin, smooth muscle alpha-actin and SM22alpha. No spontaneous calcification was observed in OPN-/- SMCs under normal culture conditions or in medium containing 1%, 3%, or 5% fetal bovine serum. However, when cultured in medium containing elevated concentrations of inorganic phosphate, an inducer of vascular calcification, a significantly higher calcification was observed in OPN-/- SMCs compared to OPN+/+ SMCs that, in response to elevated phosphate, synthesized and secreted OPN into the culture. Finally, retroviral transduction of mouse OPN cDNA into OPN-/- SMCs rescued the calcification phenotype of the cells. CONCLUSION: These results are the first to demonstrate an inhibitory role of endogenously produced OPN on SMC calcification, suggesting a novel feedback mechanism where OPN produced locally by the SMCs may serve as an important inducible inhibitor of vascular calcification.

Animals↗
PubMed1995

The vascular calcification-cutaneous necrosis syndrome.

BACKGROUND: Although medial calcification of larger elastic arteries in chronic kidney failure and with advancing age is relatively common, calcification of the cutaneous vascular system is rare. OBJECTIVE: Our purpose was to describe three patients with the vascular calcification-cutaneous necrosis syndrome and review the cause, clinical and pathologic features, and treatment of this syndrome. METHODS: We describe three patients with ischemic necrotic ulcers and underlying cutaneous vascular calcification. The clinical setting was abnormal calcium metabolism from either chronic kidney failure or excessive vitamin D intake. RESULTS: The clinical findings in all patients consisted of multiple tender livedoid nodules and ulcerative plaques on the thighs and legs, which developed in the setting of abnormal calcium metabolism from either chronic kidney failure or excessive vitamin D intake. Histologic study demonstrated vascular calcification. Although this syndrome usually has a chronic course with significant morbidity and mortality, subtotal parathyroidectomy followed by kidney transplantation resulted in complete resolution in one of our patients. CONCLUSION: The clinical and histopathologic findings in the vascular calcification-cutaneous necrosis syndrome are unique. The pathogenesis is likely multifactorial. Treatment for the skin lesions is largely supportive.

Adult↗
PubMed1999

Calcification of vascular smooth muscle cell cultures: inhibition by osteopontin.

Calcification of vascular tissue is a common complication in aging, atherosclerosis, diabetes, renal failure, aortic stenosis, and prosthetic valve replacement. Osteopontin is a noncollagenous adhesive protein routinely found at sites of dystrophic calcification and synthesized at high levels by macrophages in calcified aortic valves and atherosclerotic plaques. In the present study, we have characterized the calcification of bovine aortic smooth muscle cell (BASMC) cultures in vitro and have studied the effects of exogenous osteopontin on mineral deposition. Induction of calcification in BASMC cultures was alkaline phosphatase-dependent and was characterized by a multilayer cell morphology. Mineral deposition occurred in the basal matrix of multilayered areas as indicated by von Kossa staining, and transmission electron microscopy and electron diffraction identified the mineral as apatite. Ultrastructural analysis of the cultures showed the presence of extracellular matrix vesicles, calcifying collagen fibrils, and nodular-type calcifications similar to those found in calcified heart valves and atherosclerotic plaques. Purified osteopontin (0.05 to 5 microgram/mL) dose dependently inhibited calcification of BASMC cultures, whereas vitronectin and fibronectin had no effect. In contrast to the inhibitory mechanism of levamisole on mineral deposition, osteopontin did not inhibit alkaline phosphatase activity or reduce phosphorus levels in the culture medium. Addition of calcium to the cultures overcame the inhibitory effect of osteopontin on BASMC culture calcification and resulted in decreased levels of calcium in the culture medium and increased levels in the cell layer. Moreover, using high-resolution, colloidal-gold immunocytochemistry, osteopontin was found intimately associated with growing apatite crystals. These data indicate that the effect of osteopontin, although calcium-dependent, was not mediated by simple calcium chelation but most likely by direct interaction of osteopontin with crystal surfaces. These studies suggest that BASMCs can be used to model vascular calcification in vitro and that soluble osteopontin released near sites of vascular calcification may represent an adaptive mechanism aimed at preventing vascular calcification.

Adaptation, Physiological↗
PubMed1999

Advanced glycation endproducts accelerate calcification in microvascular pericytes.

Vascular calcification in advanced atherosclerosis is frequently associated with diabetes, and is a predictor of future cardiovascular events. To investigate the molecular mechanisms of vascular calcification, we examined whether advanced glycation endproducts (AGE) formed at an accelerated rate under diabetes induce the osteoblastic differentiation of pericytes, a mesenchymal progenitor. First, von Kossa staining demonstrated that AGE significantly increased the number of calcified nodules in a bovine pericyte culture. AGE were also found to induce calcium accumulation in the pericyte monolayer in time- and dose-dependent manners. Second, quantitative reverse transcription-polymerase chain reaction revealed that AGE increased the pericyte levels of mRNAs coding for alkaline phosphatase and osteopontin, the representative markers for early and late osteoblastic differentiation, respectively. Alkaline phosphatase activity was actually enhanced by AGE. The results suggest that AGE have the ability to induce the osteoblatic differentiation of pericytes, which would contribute to the development of vascular calcification in diabetes.

Alkaline Phosphatase↗
PubMed2002

High-density lipoprotein regulates calcification of vascular cells.

Accumulating evidence has suggested the protective role of HDL in cardiovascular disease processes. Calcification is a common feature of atherosclerotic lesions and contributes to cardiovascular complications due to the loss of aortic resilience and function. Recent studies have suggested that vascular calcification shares several features with skeletal bone formation at the cellular and molecular levels. These include the presence of osteoblast-like calcifying vascular cells in the artery wall that undergo osteoblastic differentiation and calcification in vitro. We hypothesized that HDL may also protect against vascular calcification by regulating the osteogenic activity of these calcifying vascular cells. When treated with HDL, alkaline phosphatase activity, a marker of osteogenic differentiation of osteoblastic cells, was significantly reduced in those cells. Prolonged treatment with HDL also inhibited calcification of these cells, further supporting the antiosteogenic differentiation property of HDL when applied to vascular cells. Furthermore, HDL inhibited the osteogenic activity that was induced by inflammatory cytokines interleukin (IL)-1beta and IL-6 as well as by minimally oxidized LDL. HDL also partially inhibited the IL-6-induced activation of signal transducer and activator of transcription 3 in calcifying vascular cells, suggesting that HDL may inhibit cytokine-induced signal transduction pathways. The inhibitory effects of HDL were mimicked by lipids extracted from HDL but not by HDL-associated apolipoproteins or reconstituted HDL. Furthermore, oxidation of HDL rendered it pro-osteogenic. Taken together, these results suggest that HDL regulates the osteoblastic differentiation and calcification of vascular cells and that vascular calcification may be another target of HDL action in the artery wall.

Alkaline Phosphatase↗
PubMed2005

Aortic calcification.

OBJECTIVES: Vascular calcification is a complicating factor observed in advanced atherosclerosis. This review summarises the present knowledge regarding abdominal aortic calcification. DESIGN: Literature review. METHODS: A literature review was carried using MEDLINE and PUBMED with the search terms 'abdominal', 'aortic' and 'calcification'. Articles were assessed for data regarding mechanisms, measurement, risk factors and outcomes of aortic calcification. RESULTS: Thirty relevant studies were identified. These demonstrated a positive correlation between abdominal aortic calcification and the following factors: older age, hypertension, and smoking. Further studies are required to critically assess other risk factors such as gender, diabetes mellitus and renal failure. Calcification of the abdominal aorta is associated with an increased risk of mortality, coronary heart disease and stroke. CONCLUSION: Aortic calcification predicts an increased incidence of cardiovascular events, however, the reasons for this association requires further investigation. Accurate measurement of aortic calcification is likely to be increasingly used to determine the risk of cardiovascular events.

Age Factors↗
PubMed2006

Premature induction of hypertrophy during in vitro chondrogenesis of human mesenchymal stem cells correlates with calcification and vascular invasion after ectopic transplantation in SCID mice.

OBJECTIVE: Functional suitability and phenotypic stability of ectopic transplants are crucial factors in the clinical application of mesenchymal stem cells (MSCs) for articular cartilage repair, and might require a stringent control of chondrogenic differentiation. This study evaluated whether human bone marrow-derived MSCs adopt natural differentiation stages during induction of chondrogenesis in vitro, and whether they can form ectopic stable cartilage that is resistant to vascular invasion and calcification in vivo. METHODS: During in vitro chondrogenesis of MSCs, the expression of 44 cartilage-, stem cell-, and bone-related genes and the deposition of aggrecan and types II and X collagen were determined. Similarly treated, expanded articular chondrocytes served as controls. MSC pellets were allowed to differentiate in chondrogenic medium for 3-7 weeks, after which the chondrocytes were implanted subcutaneously into SCID mice; after 4 weeks in vivo, samples were evaluated by histology. RESULTS: The 3-stage chondrogenic differentiation cascade initiated in MSCs was primarily characterized by sequential up-regulation of common cartilage genes. Premature induction of hypertrophy-related molecules (type X collagen and matrix metalloproteinase 13) occurred before production of type II collagen and was followed by up-regulation of alkaline phosphatase activity. In contrast, hypertrophy-associated genes were not induced in chondrocyte controls. Whereas control chondrocyte pellets resisted calcification and vascular invasion in vivo, most MSC pellets mineralized, in spite of persisting proteoglycan and type II collagen content. CONCLUSION: An unnatural pathway of differentiation to chondrocyte-like cells was induced in MSCs by common in vitro protocols. MSC pellets transplanted to ectopic sites in SCID mice underwent alterations related to endochondral ossification rather than adopting a stable chondrogenic phenotype. Further studies are needed to evaluate whether a more stringent control of MSC differentiation to chondrocytes can be achieved during cartilage repair in a natural joint environment.

Adult↗
PubMed2005

Calcification and cardiovascular problems in renal failure.

Extraosseus calcification has plagued management of renal failure since the beginning of hemodialysis, but the issue has largely been neglected because the impact on survival was thought to be limited. The recent recognition that hyperphosphatemia is a strong predictor of all-cause mortality, and particularly of cardiac mortality, has transformed the situation. Relatively stringent, though difficult to implement, guidelines have been proposed for the management of hyperphosphatemia. Important recent insights document that, for different reasons, both high and low turnover of bone disease increase the risk of vascular calcifications. Vascular calcification impacts cardiac death not only by complicating coronary atherosclerosis, but also by increasing the stiffness of central arteries, impacting on heart function (increased impedance, reduced coronary perfusion). While in the past extraosseous calcification, including vascular calcification, was thought to be a passive process resulting from transgression of a critical Ca x P product, recent studies show that the adverse effect of hyperphosphatemia is also mediated by active processes (e.g., induction of "osteogenic" genetic programs), and is modulated by calcification inhibitors.

Calcinosis↗
PubMed2005

Optical measurement of age-related calcification in human blood vessels.

Vascular calcification is commonly associated with aging. Quantification of calcium accumulation in vessel walls is important in understanding the mechanisms of vascular calcification. To elucidate age-related change of calcification, site dependence of calcification, and the effect of hemodynamic stress on calcification, we measured calcium contents in various blood vessels with atomic emission spectrometry and simulated blood flow in the vessels by computational fluid dynamics. The content of calcium in the arteries increased progressively with aging while there is no change in the veins. The higher accumulation of calcium occurred in the arteries of the lower limb in comparison to the arteries of the upper limb. In the arterial bifurcation, there was the correlation at hemodynamic stress distribution and calcium content. The results of this study quantitatively support clinical findings of nonuniform calcification, and suggest that hemodynamic stress affects vascular calcification.

Age Factors↗
PubMedDate not supplied

Elevated leg systolic pressures and arterial calcification in diabetic occlusive vascular disease.

Systolic occlusion leg and brachial pressures were determined using a Doppler ultrasonic method in 24 diabetic subjects with either past or evolving gangrene due to arterial occlusive disease of the lower extremities. The leg-brachial ratios were correlated with x-ray determined leg vascular calcification. Ratios above 1.10 were invariably associated with heavy continuous calcification of the tibial vessels; lesser degrees of arterial calcification had normal or depressed leg-brachial ratios. Medial calcification might be causally related to the abnormally elevated leg systolic pressures not infrequently noted in diabetic patients. Based on the observed occurrence of reamputation in association with normal or elevated leg-brachial ratios, it appears that a Doppler pressure index above 0.90 is not a reliable indicator of adequate blood flow in severe diabetic occlusive arterial disease.

Aged↗
PubMed2006

Mammography as a screening tool for peripheral vascular disease.

BACKGROUND: Peripheral vascular disease (PVD) is a progressive and debilitating disease often diagnosed only when patients become symptomatic. Currently there are no widespread screening tests available for the early detection of PVD. Patients with diabetes and coronary artery disease are known to have a higher incidence of PVD. Prior studies have indicated that benign vascular calcifications seen on routine screening mammogram are more prevalent in women with diabetes and coronary artery disease. The same association has not been shown for women with PVD. The purpose of this study was to identify an association between benign vascular calcifications identified on mammography and PVD. If such an association exists then screening mammography, already widely used as a screening tool for breast cancer, may identify women at high risk for PVD. METHODS: To determine the incidence of vascular calcifications in our general screening population we prospectively evaluated consecutive routine screening mammograms for the presence of benign vascular calcifications. We then identified a population of women with PVD by using a computerized database maintained by the Division of Vascular Surgery. The population of women identified with PVD was categorized further to identify those women who had received routine screening mammogram within our hospital system. These mammograms were reviewed retrospectively with particular attention to the presence of vascular calcifications. All mammograms were reviewed by our dedicated mammographers. Statistical analysis of the study group using the chi-square test was performed to determine the association of PVD and mammographic vascular calcifications. RESULTS: Prospective evaluation of 645 women undergoing consecutive routine screening mammography identified 123 (19%) with benign vascular calcifications. By using our PVD computerized database between the years 2002 and 2004 we identified 763 women with PVD. Of this group only 121 (15%) had undergone a routine screening mammogram in our hospital system. These mammograms were reviewed retrospectively by the same group evaluating the screening mammograms. On evaluation vascular calcifications were identified in 42% (51 of 121) of these women with PVD. Statistical analysis was performed using the chi-square test, odds ratio, and relative risk. A highly significant association was identified between PVD and the presence of mammographic vascular calcifications (P > .001). With a confidence interval of 95% the presence of benign vascular microcalcifications on routine screening mammogram identifies a significant risk for PVD with an odds ratio of 3.06. We showed through our analysis that women with calcifications are 2.19 times more likely to have PVD if microcalcifications are present. By using vascular calcifications identified on screening mammography as a means to identify women with PVD the sensitivity and specificity are 42% and 80%, respectively. The positive predictive value and the negative predictive value are 29% and 88%, respectively, with an accuracy of 75%. CONCLUSIONS: This initial study indicates that the presence of vascular calcifications identified on routine screening mammogram is significantly higher in women with PVD and the lack of vascular calcifications on screening mammography correlates well with a negative history of PVD. We have identified a significant association with PVD and vascular calcifications in our patient population. Further studies are indicated to determine if screening mammography may become a widespread inexpensive screening tool to identify women at risk for PVD. Additional studies are underway at our institution to evaluate the association of PVD, diabetes and coronary artery disease, and vascular calcifications identified on routine screening mammography.

Adult↗
PubMed2007

Calcifications, arterial stiffness and atherosclerosis.

UNLABELLED: Vascular calcification can occur in either the intimal or medial layers of the arterial wall. Intimal calcification is associated with atherosclerosis, which is characterized by lipid accumulation, inflammation, fibrosis and development of focal plaques. Medial calcification is associated with arterio sclerosis, i.e. age- and metabolic disease-related structural changes in the arterial wall which are related to increased arterial stiffness. It has been hypothesized that vascular calcification, either intimal or medial, may directly increase arterial stiffness. Alternatively, arterial stiffness may contribute to the development of calcification and focal plaque. Ample evidence (i.e. animal data and studies of diabetes and end-stage renal disease) has demonstrated that medial calcification of elastic fibers contributes to increased arterial stiffness. Evidence linking intimal calcification with arterial stiffness is less definitive, partly because it is very difficult to differentiate vascular calcification due to focal plaques (intimal) from medial calcification, and partly because the number of studies has been small. CONCLUSION: Current evidence supports that medial calcification is associated with increases in arterial stiffness. The association between intimal (atherosclerotic-associated) calcification and arterial stiffness is less definitive.

Aortic Diseases↗
PubMed1998

In vitro and in vivo calcification of vascular bioprostheses.

Efficacy of different chemical treatments on calcification of vascular graft in vitro and in vivo was studied. Culture medium-filled rat aortas were separately treated in 0.2% glutaraldehyde and epoxy compound, and photooxidized in 0.01% methylene blue for a shorter period (group 1). Another group of rat aortas were separately treated in the same chemicals for a longer period (group 2). All fresh and treated aortas of both groups were cultured for 21 days in an organ culture medium and implanted (except for group 1) in weanling rats for five months. Histology and immunohistochemistry revealed that differently treated aortas of group 1 grow and calcify, and the smooth muscle cells between elastin fibers are the primary site of calcium deposition. In contrast, differently treated aortas of group 2 neither grew, nor did calcify in the medium except the epoxy compound cross-linked aorta of group 2 which did not grow but did calcify. Untreated aorta did not calcify. All fresh and differently treated aortic homografts calcified severely in rats. Our whole arterial segment-calcification system would be useful for analyzing the molecular and cellular mechanisms of both bioprosthetic and atherosclerotic calcification of vascular graft. New anticalcification technique is the only hope for better outcome of future vascular bioprostheses.

Animals↗
PubMed2006

Pulmonary hypertension in chronic dialysis patients with arteriovenous fistula: pathogenesis and therapeutic prospective.

PURPOSE OF REVIEW: End-stage renal disease patients receiving chronic haemodialysis via arteriovenous access often develop various cardiovascular complications, including vascular calcification, cardiac-vascular calcification and atherosclerotic coronary disease. This review describes recently published studies that demonstrate a high incidence of pulmonary hypertension among patients with end-stage renal disease receiving long-term haemodialysis via a surgical arteriovenous fistula. Both end-stage renal disease and long-term haemodialysis via arteriovenous fistula may be involved in the pathogenesis of pulmonary hypertension by affecting pulmonary vascular resistance and cardiac output. RECENT FINDINGS: Morbidity and mortality from cardiovascular disease are greatly increased in patients on maintenance haemodialysis therapy. Using Doppler echocardiography, we found a significant increase in cardiac output in 40% of chronic haemodialysis patients, probably related to the large arteriovenous access or altered vascular resistance as a result of the local vascular tone and function expressed by the imbalance between vasodilators such as nitric oxide, and vasoconstrictors such as endothelin-1. SUMMARY: We propose different potential mechanisms as explanations for the development of pulmonary hypertension. Hormonal and metabolic derangement associated with end-stage renal disease might lead to pulmonary arterial vasoconstriction and an increase in pulmonary vascular resistance. Pulmonary arterial pressure may be further increased by high cardiac output resulting from the arteriole-venous access itself, worsened by commonly occurring anaemia and fluid overload.

Adult↗