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Biomedical subjects

H Oda

Publications and source records attributed to H Oda.

At least 109 records · Page 6Linked to original sources
PubMed1999

Different frequencies of p53 codon-249 hot-spot mutations in hepatocellular carcinomas in Jiang-su province of China.

Environmental carcinogens often induce specific mutations in the p53 gene, apparent in tumors. The relation between aflatoxin B1 (AFB1 )-related hepatocellular carcinomas (HCCs) and hot spot at codon 249 of the p53 gene has received a great deal of attention, but its significance is still controversial. To clarify this problem, we analyzed the p53-mutational status of HCCs in Jiang-su province in China, where AFB1 contamination of the staple food significantly differs between the northern and southern parts (prominent only in the latter), while other conditions are quite similar. Background liver status and mutations in exons 5 to 8 of p53 in a total of 31 cases were divided approximately equally between the 2 areas. In all, 15 tumors exhibited a total of 17 mutations in the p53 gene; 9 cases from the southern part of the province had the hot-spot mutation at codon 249 (9/16, 56%), but only one case from the northern part (1/15, 8%). These results suggest that AFB1 contamination may correlate with codon-249 mutations in HCC.

Adult↗
PubMed1999

Expression of E2A-HLF chimeric protein induced T-cell apoptosis, B-cell maturation arrest, and development of acute lymphoblastic leukemia.

The E2A-HLF fusion gene, generated by t(17;19)(q22;p13) in acute lymphoblastic leukemia (ALL), encodes a chimeric transcription factor in which the trans-activating domains of E2A are fused to the DNA-binding and dimerization domains of hepatic leukemic factor (HLF). To investigate its biological role, we generated transgenic mice expressing E2A-HLF using Ig enhancer and promoter, which direct transgene expression in cells committed to the lymphoid lineage. The transgenic mice exhibited abnormal development in the thymus and spleen and were susceptible to infection. The thymus contained small numbers of thymocytes, and TUNEL staining showed that higher population of thymocytes were undergoing apoptosis. The spleen exhibited a marked reduction in splenic lymphocytes and the flow cytometric analyses and the in vitro colony formation assays showed that the B-cell maturation was blocked at a very early developmental stage. These findings indicated that the expression of E2A-HLF induced T-cell apoptosis and B-cell maturation arrest in vivo and that the susceptibility of the transgenic mice to infection was due to immunodeficiency. Moreover, several transgenic mice developed acute leukemia, classified as T-ALL based on the surface marker analysis and DNA rearrangements, suggesting that an additional event is required for malignant transformation of lymphoid cells expressing E2A-HLF. Our findings provide insight into the biological function of E2A-HLF in lymphoid development and also its role in leukemogenesis.

Adenovirus E2 Proteins↗
PubMed1999

Actin dynamics in lamellipodia of migrating border cells in the Drosophila ovary revealed by a GFP-actin fusion protein.

Directional migration of border cells in the Drosophila egg chambers is a developmentally regulated event that requires dynamic cellular functions. In this study, the electron microscopic observation of migrating border cells revealed loose actin bundles in forepart lamellipodia and numerous microvilli extending from nurse cells and providing multiple adhesive contacts with border cells. To analyze the dynamics of actin in migrating border cells in vivo, we constructed a green fluorescent protein-actin fusion protein and induced its expression in Drosophila using the GAL4/UAS system. The green fluorescent protein-actin was incorporated into the actin bundles and it enabled visualization of the rapid cytoskeletal changes in border cell lamellipodia. During the growth of the lamellipodia, the actin bundles that increased in number and size radiated from the bundle-organizing center. Quantification of the fluorescence intensity showed that an accumulation of bundle-associated and spotted green fluorescent protein-actin signals took place during their centripetal movement. Our results favored a treadmilling model for actin behavior in border cell lamellipodia.

Actins↗
PubMed1999

A case of thrombopoietin-producing ovarian carcinoma confirmed by immunohistochemistry.

A case of ovarian carcinoma with thrombopoietin production is reported. A 49-year-old Japanese woman had serous cystadenocarcinoma of the right ovary with peritoneal spread. The platelet count was elevated to 432 x 10(9)/L. Enzyme-linked immunosorbent assay of the serum demonstrated remarkably high levels of thrombopoietin (2.96 fmol/ml). Immunohistochemical examination using an antibody specific for thrombopoietin revealed positive staining in the carcinoma cells, confirming thrombopoietin production.

Cystadenocarcinoma, Serous↗
PubMed1999

Live Bartonella henselae enhances endothelial cell proliferation without direct contact.

The proliferation of human umbilical vein endothelial cells (HUVECs) cocultivated with live B. henselae was enhanced in a bacterial dose-dependent manner, and the stimulatory effect was specific to vascular endothelial cells. The inactivation of B. henselae by UV or heat treatment abolished its stimulatory activity, suggesting that live bacteria is necessary for the growth stimulation effect. To investigate the role of direct contact, live B. henselae were separated from HUVECs by a filter membrane (Millicell-CM insert). Even under this condition, an enhanced proliferation of HUVECs was observed. However, no morphological changes in the HUVECs were apparent compared to the B. henselae -infected cells. Furthermore, we isolated a nonpiliated strain of B. henselae that is unable to attach to and enter into endothelial cells. The nonpiliated strain possessed the ability to stimulate the proliferation of cocultivated HUVECs the same as the piliated strain. Moreover, the culture supernatants of B. henselae were also able to induce HUVEC proliferation. Our results indicate that the stimulation of HUVEC proliferation by B. henselae is mediated by soluble factor(s) secreted from the bacteria.

Angiomatosis, Bacillary↗
PubMed1999

Preoperative detection of occult enterovesical fistulas in patients with Crohn's disease: efficacy of oral or rectal administration of indocyanine green solution.

OBJECTIVES: Nonhazardous enteral administration of indocyanine green solution was performed to detect enterovesical occult microfistulas in patients with Crohn's disease before the fistulas had become readily apparent. METHODS: A total of 12 patients with Crohn's disease who were suspected from their clinical manifestations of having enterovesical fistulas underwent study. For detection of the fistulas after oral or rectal administration of the indocyanine green solution, urine was collected and examined using a colorimeter to check for contamination with indocyanine green. The effectiveness of the indocyanine green test and conventional x-ray study was compared. RESULTS: The indocyanine green test was positive after either oral or rectal administration in 11 of the 12 patients, providing a rate of accurate diagnosis of 92 percent (11/12 patients). In contrast, the rate of accurate diagnosis using the x-ray study was only 17 percent (2/12 patients). Furthermore, in eight patients with occult fistulas, accurate diagnosis could be made in none using the x-ray study, whereas all showed positive results with use of the indocyanine green test. CONCLUSIONS: The ability to diagnose obscure fistulas using the indocyanine green test was 92 percent. This indocyanine green test was highly diagnostic, whereas conventional examinations are often complicated and much less diagnostic.

Administration, Oral↗
PubMed1999

Spontaneous subcapital femoral neck fracture complicating a healed intertrochanteric fracture.

A spontaneous subcapital femoral neck fracture is an uncommon complication of a healed intertrochanteric hip fracture. To determine the etiology of this complication, 274 patients who had been treated for intertrochanteric hip fractures were followed up over an 8-year period from June 1988 to June 1996. We found 7 fractures of the subcapital femoral neck without a history of a trauma. The remaining 267 patients were defined as the control group. All seven patients with fractures of the subcapital femoral neck were women, and their average age at the time of compression hip screw (CHS) fixation was 83 years (range 74-92 years). The subcapital fractures occurred between 4 and 36 months after CHS fixation. The difference in the Singh index between the patient and control groups was statistically significant (P < 0.01). However, with regard to the position of the screw, spinal score, age, ambulatory ability, height, weight, and intertrochanteric fracture type (Jensen type), the differences between the patient and control groups were not statistically significant. Based on our findings, we conclude that a high grade of osteoporosis is the most important predisposing factor in the spontaneous development of a subcapital femoral neck fracture after a healed intertrochanteric hip fracture.

Aged↗
PubMed1999

Dynamic features of adherens junctions during Drosophila embryonic epithelial morphogenesis revealed by a Dalpha-catenin-GFP fusion protein.

Cell-cell adherens junctions (AJs), comprised of the cadherin-catenin adhesion system, contribute to cell shape changes and cell movements in epithelial morphogenesis. However, little is known about the dynamic features of AJs in cells of the developing embryo. In this study, we constructed Dalpha-catenin fused with a green fluorescent protein (Dalpha-catenin-GFP), and found that it targeted apically located AJ-based contacts but not other lateral contacts in epithelial cells of living Drosophila embryos. Using time-lapse fluorescence microscopy, we examined the dynamic performance of AJs containing Dalpha-catenin-GFP in epithelial morphogenetic movements. In the ventral ectoderm of stage 11 embryos, concentration and deconcentration of Dalpha-catenin-GFP occurred concomitantly with changes in length of AJ contacts. In the lateral ectoderm of embryos at the same stage, dynamic behaviour of AJs was concerted with division and delamination of sensory organ precursor (SOP) cells. Moreover, changes in patterns of AJ networks during tracheal extension could be followed. Finally, we utilized Dalpha-catenin-GFP to precisely observe the defects in tracheal fusion in shotgun mutants. Thus, the Dalpha-catenin-GFP fusion protein is a helpful tool to simultaneously observe morphogenetic movements and AJ dynamics at high spatio-temporal resolution.

Animals↗
PubMed1999

Inhibition of noradrenaline release from PC12 cells by the long-term treatment with cholera toxin.

Guanine nucleotide-binding (G) proteins are required for intracellular vesicular transport and endocytosis. In this study, we investigated the effects of short-term (2 h) and long-term (24 h) treatment with cholera toxin (CTX), which ADP-ribosylates proteins having arginine residues such as the alpha subunit of Gs (G(s alpha)), on exocytosis from the neurosecretory rat pheochromocytoma PC 12 cell line. Short-term treatment with CTX stimulated the accumulation of cyclic AMP, and synergistically enhanced both extracellular Ca2+-dependent [3H]noradrenaline (NA) releases (induced by high K+ and ATP) and Ca2+-independent release (induced by mastoparan, a peptide in wasp venom). Long-term treatment with CTX for 24h inhibited Ca2+-dependent and -independent stimulated [3H]NA release. The inhibitory effect of long-term CTX treatment was not derived from a cyclic AMP-dependent system, because (1) H-89, an inhibitor of protein kinase A, had no effect on the inhibition induced by CTX, (2) the long-term treatment with forskolin did not show an inhibitory effect. [32P]ADP-ribosylation of G(s alpha) and its immunoreactivity with anti-G(s alpha) antiserum in the crude membrane fraction was inhibited in the long-term CTX-treated cells, but not in the long-term forskolin-treated cells. [32P]ADP-ribosylation of G(s alpha) in the membrane fraction of short-term CTX-treated cells was approximately 90% of the level in the control cells. These findings suggest that CTX stimulates [3H]NA release via a cyclic AMP-dependent system in the short-term, and that long-term CTX treatment inhibited its release, maybe via ADP-ribosylation of CTX-sensitive proteins such as G(s alpha).

Adenosine Diphosphate Ribose↗
PubMed1999

Effects of adjunctive balloon angioplasty after intravascular ultrasound-guided optimal directional coronary atherectomy: the result of Adjunctive Balloon Angioplasty After Coronary Atherectomy Study (ABACAS).

OBJECTIVES: This study was conducted to evaluate: 1) the effect of adjunctive percutaneous transluminal coronary angioplasty (PTCA) after directional coronary atherectomy (DCA) compared with stand-alone DCA, and 2) the outcome of intravascular ultrasound (IVUS)-guided aggressive DCA. BACKGROUND: It has been shown that optimal angiographic results after coronary interventions are associated with a lower incidence ofrestenosis. Adjunctive PTCA after DCA improves the acute angiographic outcome; however, long-term benefits of adjunctive PTCA have not been established. METHODS: Out of 225 patients who underwent IVUS-guided DCA, angiographically optimal debulking was achieved in 214 patients, then theywere randomized to either no further treatment or to added PTCA. RESULTS: Postprocedural quantitative angiographic analysis demonstrated an improved minimum luminal diameter (2.88 +/- 0.48 vs. 2.6 +/- 0.51 mm; p = 0.006) and a less residual stenosis (10.8% vs.15%; p = 0.009) in the adjunctive PTCA group. Quantitative ultrasound analysis showed a larger minimum luminal diameter (3.26 +/- 0.48 vs. 3.04 +/- 0.5 mm; p < 0.001) and lower residual plaque mass in the adjunctive PTCA group (42.6% vs. 45.6%; p < 0.001). Despite the improved acute findings in the adjunctive PTCA group, six-month angiographic and clinical results were not different. The restenosis rate (adjunctive PTCA 23.6%, DCA alone 19.6%; p = ns) and target lesion revascularization rate (20.6% vs. 15.2%; p = ns) did not differ between the groups. CONCLUSIONS: With IVUS guidance, aggressive DCA can safely achieve optimal angiographic results with low residual plaque mass, and this was associated with a low restenosis rate. Although adjunctive PTCA after optimal DCA improved the acute quantitative coronary angiography and quantitative coronary ultrasonography outcomes, its benefit was not maintained at six months.

Aged↗
PubMed1999

Glucocorticoid-dependent induction of HMG-CoA reductase and malic enzyme gene expression by polychlorinated biphenyls in rat hepatocytes.

Administration of xenobiotics to rats results in hypercholesterolemia and in the induction of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and malic enzyme. To investigate the mechanism of the induction of the enzymes by xenobiotics, the effects of xenobiotics on gene expressions for HMG-CoA reductase, malic enzyme, and cytochrome P-450 in rat liver and in cultured hepatocyte were investigated. The treatment of rats with polychlorinated biphenyls (PCB) as a xenobiotic induced mRNAs for HMG-CoA reductase and malic enzyme as well as CYP2B1/2 (cytochrome P-450b/e). Other xenobiotics, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT), and chloretone, also increased HMG-CoA reductase mRNA. In an investigation of diurnal rhythm of mRNA for HMG-CoA reductase, the induction by PCB was observed in a dark period. Induced expressions of HMG-CoA reductase gene and malic enzyme gene by PCB were observed in primary cultured rat hepatocytes and showed that the action of PCB on the gene expression relating to lipid metabolism was directed on hepatocytes. The induction was observed only in hepatocytes cultured on Engelbreth-Holm-Swarm sarcoma basement membrane gel (EHS-gel), not on type I collagen, which is usually used for monolayer culture of hepatocytes. The induction of CYP2B1/2 gene expression also was observed only in the cells cultured on EHS-gel. The induction of HMG-CoA reductase and malic enzyme by PCB required dexamethasone. However, the addition of dexamethasone per se to medium containing insulin did not show an inductive effect on levels of mRNA for HMG-CoA reductase and malic enzyme. From the data of diurnal variation and hepatocyte culture experiment, HMG-CoA reductase and malic enzyme are considered to be induced by PCB through the so-called "permissive effect" of glucocorticoid.

Journal Article↗
PubMed1999

Increased insulin sensitivity and hypoglycaemia in mice lacking the p85 alpha subunit of phosphoinositide 3-kinase.

The hallmark of type 2 diabetes, the most common metabolic disorder, is a defect in insulin-stimulated glucose transport in peripheral tissues. Although a role for phosphoinositide-3-kinase (PI3K) activity in insulin-stimulated glucose transport and glucose transporter isoform 4 (Glut4) translocation has been suggested in vitro, its role in vivo and the molecular link between activation of PI3K and translocation has not yet been elucidated. To determine the role of PI3K in glucose homeostasis, we generated mice with a targeted disruption of the gene encoding the p85alpha regulatory subunit of PI3K (Pik3r1; refs 3-5). Pik3r1-/- mice showed increased insulin sensitivity and hypoglycaemia due to increased glucose transport in skeletal muscle and adipocytes. Insulin-stimulated PI3K activity associated with insulin receptor substrates (IRSs) was mediated via full-length p85 alpha in wild-type mice, but via the p50 alpha alternative splicing isoform of the same gene in Pik3r1-/- mice. This isoform switch was associated with an increase in insulin-induced generation of phosphatidylinositol(3,4,5)triphosphate (PtdIns(3,4,5)P3) in Pik3r1-/- adipocytes and facilitation of Glut4 translocation from the low-density microsome (LDM) fraction to the plasma membrane (PM). This mechanism seems to be responsible for the phenotype of Pik3r1-/- mice, namely increased glucose transport and hypoglycaemia. Our work provides the first direct evidence that PI3K and its regulatory subunit have a role in glucose homeostasis in vivo.

Animals↗
PubMed1999

Recent advances in statins and the kidney.

BACKGROUND: Experimental and clinical studies have suggested a correlation between the progression of renal disease and dyslipidemia. Indeed, apolipoprotein B-containing lipoproteins have been demonstrated to be an independent risk factor for the progression of renal disease in humans. Interventional strategies in experimental models of renal disease have clearly demonstrated a beneficial effect on renal structure and function in a variety of models of renal disease. Investigations into the mechanisms whereby reduction of lipids by lipid-lowering agents benefits renal disease have suggested that the 3-hydroxy-3-methylglutaryl coenzyme reductase inhibitors, the so-called statin class of lipid-lowering agents, may have additional effects on the biology of inflammation that are germane to the progression of renal disease. METHODS: Both in vivo and in vitro studies that investigated secondary mechanisms of statin effects are reviewed. In addition, new studies that investigated the effects on novel cellular mechanisms are presented. RESULTS: Lipid-lowering agents appear to have biologically important effects in modulating a variety of intracellular signaling systems involved in cell proliferation, inflammatory responses that involve macrophage adhesion, recruitment, and maturation. In addition, the effects on fibrogenesis have been recently defined. These latter effects may influence not only the development of glomerulosclerosis, but also interstitial fibrosis. These potentially major effects of lipid-lowering agents appear to be related to the effects on intracellular synthesis of nonsterol isoprenoids, which are involved in prenylation of critical small molecular weight proteins involved in cell signal transduction. CONCLUSIONS: In addition to the beneficial effects of the reduction in serum lipids, statins and other lipid-lowering agents may influence important intracellular pathways that are involved in the inflammatory and fibrogenic responses, which are common components of many forms of progressive renal injury.

Animals↗
PubMed1999

Apolipoprotein E polymorphism and renal disease.

BACKGROUND: Lipid abnormalities are frequently found in end-stage renal disease (ESRD), and abnormal lipid metabolism may contribute to the progression of renal disease. Previous investigators have reported that apolipoprotein E (apoE) has an important role in lipoprotein metabolism and that the process of lipoprotein catabolism varies according to the apoE phenotype. In addition, the relative frequency of the apoE alleles is different among the races. In this study, we investigated the allele frequency of apoE phenotypes and evaluated the impact of apoE polymorphism on lipid profile in Japanese patients with renal disease. METHODS: ApoE phenotypes were determined using isoelectric focusing and Western blotting in 592 Japanese patients with renal disease [86 out of 107 patients with glomerulonephritis had proteinuria of not less than 0.25 g per 24 hr and 485 with ESRD; 448 were on hemodialysis (HD), and 37 were on continuous ambulatory peritoneal dialysis (CAPD)]. The allele frequency and apoE phenotype distribution were estimated by the gene-counting method. Serum lipid parameters related to lipid metabolism were measured after at least a 12-hour fast. RESULTS: The allele frequency of the three major apoE phenotypes (apoE2, apoE3, and apoE4) in 107 glomerulonephritis patients (epsilon 2; 0.037, epsilon 3; 0.860, epsilon 4; 0.103) was almost identical to that in the normal control population (epsilon 2; 0.036, epsilon 3; 0.848, epsilon 4; 0.115). However, 86 glomerulonephritis patients with proteinuria had higher allele frequency of apoE2 (epsilon 2; 0.052, P < 0.01) and apoE4 (epsilon 4; 0.140, P < 0.001) and lower allele frequency of apoE3 (epsilon 3; 0.808, P < 0.001) than the controls. Furthermore, ESRD patients had higher allele frequency of apoE2 (epsilon 2; 0.058, P < 0.01) and lower allele frequency of apoE4 (epsilon 4; 0.091, P < 0.05) than the controls. Higher prevalence of nephrotic syndrome was found in proteinuric glomerulonephritis patients with apoE2. The impact of apoE polymorphism on serum lipid profile in patients with glomerulonephritis, HD, and CAPD was different from that generally expected. CONCLUSIONS: The higher frequency of apoE2 in ESRD patients suggests that apoE2 is a possible genetic predisposition to ESRD in a Japanese population. The impact of apoE2 and apoE4 on lipid profile in patients with renal disease was unique and different from that in the normal population.

Alleles↗
PubMed1999

Effect of lipoproteins on mesangial cell proliferation.

BACKGROUND: Triglyceride (TG)-rich lipoproteins have been reported to promote atherosclerosis, but little is known about their role in kidney disease or about their effects on mesangial cells. Accordingly, the purpose of this study was to investigate which lipoproteins could influence mesangial cell proliferation in vitro. We assessed the effect of various lipoproteins [very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low density lipoprotein (LDL), oxidized LDL, and high-density lipoprotein (HDL)] on the proliferation of cultured human mesangial cells and also assessed the influence of these lipoproteins on cytokine production. METHODS: We investigated the effect of various lipoproteins on cultured human mesangial cells using 3H-thymidine incorporation and cell counting assays and investigated the levels of several cytokines [interleukin (IL)-6, platelet-derived growth factor (PDGF), transforming growth factor (TGF)-beta, and tumor necrosis factor-alpha] in mesangial cell culture supernatants after stimulation by the lipoproteins. RESULTS: Not only LDL but also TG-rich lipoproteins (VLDL and IDL) promoted the proliferation of mesangial cells up to certain concentrations, but cell growth was actually decreased at higher concentrations. Oxidized LDL caused a concentration-dependent decrease of 3H-thymidine incorporation, and HDL had no proliferative effect at any concentration. Exposure to VLDL, IDL, LDL, or a high concentration of HDL enhanced the secretion of IL-6, PDGF-AB, and TGF-beta by mesangial cells, whereas TNF-alpha secretion was stimulated by oxidized LDL. CONCLUSIONS: TG-rich lipoproteins, LDL, and oxidized LDL may be involved in mesangial cell proliferation and injury in patients with mesangial proliferative glomerulonephritis.

Cell Division↗
PubMed1999

Effects of lovastatin on expression of cell cycle regulatory proteins in vascular smooth muscle cells.

BACKGROUND: The sequential appearance of cyclins D and E is thought to initiate subsequent DNA synthesis in proliferating cells. Previous studies have reported that DNA synthesis in cultured rat vascular smooth muscle cells (VSMCs) was suppressed by the HMG-CoA reductase inhibitor lovastatin. The effects of lovastatin on cell cycle regulatory proteins in proliferating VSMCs, however, are largely unknown. Thus, we investigated the sequential expression of cyclin D1, cyclin E, cyclin-dependent kinase (CDK) 4, CDK2, and p27Kip1 in cultured rat VSMCs stimulated by platelet-derived growth factor (PDGF)-BB in the presence or absence of lovastatin. METHODS: Quiescent VSMCs, with and without lovastatin (20 microM) pretreatment for nine hours, were stimulated by PDGF-BB (25 ng/ml). The incorporation of tritiated thymidine was done to assess DNA synthesis. VSMC lysates were obtained every 6 hours for up to 36 hours after stimulation and were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis using relevant polyclonal antibodies. Autoradiograms were analyzed using a densitometer. RESULTS: The peak expression of cyclins D1 and E occurred at 18 and 30 hours of PDGF stimulation, respectively. Concomitant expression of CDK4 and CDK2 was also observed. The expression of p27Kip1, by contrast, was reduced in association with DNA synthesis. Lovastatin suppressed DNA synthesis and reduced the expression of cyclin D1 and cyclin E, whereas p27Kip1 expression was strongly induced by lovastatin pretreatment. CDK4 and CDK2 expression was unaffected by lovastatin treatment. CONCLUSIONS: PDGF-BB induces cyclins D1 and E prior to the onset of DNA synthesis in VSMCs. Lovastatin may suppress DNA synthesis in VSMCs by inducing p27Kip1 and reducing expression of cyclins D1 and E.

Animals↗
PubMed1999

Lipoprotein(a) as a risk factor for coronary artery disease in hemodialysis patients.

BACKGROUND: We studied whether lipoprotein(a) [Lp(a)] is an independent risk factor for coronary artery disease (CAD) in hemodialysis (HD) patients. METHODS: A serum concentration of Lp(a) was measured in 212 patients with chronic glomerulonephritis and 56 patients with diabetic nephropathy (a total of 268 patients). The causes of death during five years of follow-up were studied and classified into either cardiovascular or noncardiovascular events. RESULTS: The mortality of these 268 HD patients during the observation period was 26.1%. Seventy-eight percent were due to cardiovascular events. Those who died of cardiovascular events had significantly higher serum Lp(a) levels than those died of noncardiovascular events. The relative risk of death from CAD was 0.71 in HD patients with a Lp(a) concentration above 30 mg/dl. CONCLUSIONS: This study indicates that the serum Lp(a) levels are independent indicators of the future risk of death from CAD in HD patients.

Adult↗