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Lindström, S. B., Uhlin, F., Bjarnegård, N., Gylling, M., Nilsson, K., Svensson, C., . . . Länne, T. (2018). Computer-Aided Evaluation of Blood Vessel Geometry From Acoustic Images. Journal of ultrasound in medicine, 37(4), 1025-1031
Open this publication in new window or tab >>Computer-Aided Evaluation of Blood Vessel Geometry From Acoustic Images
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2018 (English)In: Journal of ultrasound in medicine, ISSN 0278-4297, E-ISSN 1550-9613, Vol. 37, no 4, p. 1025-1031Article in journal (Refereed) Published
Abstract [en]

A method for computer-aided assessment of blood vessel geometries based on shape-fitting algorithms from metric vision was evaluated. Acoustic images of cross sections of the radial artery and cephalic vein were acquired, and medical practitioners used a computer application to measure the wall thickness and nominal diameter of these blood vessels with a caliper method and the shape-fitting method. The methods performed equally well for wall thickness measurements. The shape-fitting method was preferable for measuring the diameter, since it reduced systematic errors by up to 63% in the case of the cephalic vein because of its eccentricity.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2018
Keyword
blood vessel wall, computer-aided assessment, informatics/image processing, lumen diameter, peripheral vascular, shape fitting
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-144016 (URN)10.1002/jum.14439 (DOI)29027696 (PubMedID)
Available from: 2018-01-03 Created: 2018-01-03 Last updated: 2018-04-11Bibliographically approved
Vorkapic, E., Folkesson, M., Magnell, K., Bohlooly-Y, M., Länne, T. & Wågsäter, D. (2017). ADAMTS-1 in abdominal aortic aneurysm. PLoS ONE, 12(6), Article ID e0178729.
Open this publication in new window or tab >>ADAMTS-1 in abdominal aortic aneurysm
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2017 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 12, no 6, article id e0178729Article in journal (Refereed) Published
Abstract [en]

INTRODUCTION: Extracellular matrix degradation is a hallmark of abdominal aortic aneurysm (AAA). Among proteases that are capable of degrading extracellular matrix are a disintegrin and metalloproteases with thrombospondin motifs (ADAMTS). Pathogenesis of these proteases in AAA has not been investigated until date.

METHODS AND RESULTS: Human aneurysmal and control aortas were collected and analyzed with RT-PCR measuring the ADAMTS-1, 4,5,6,8,9,10,13,17 and ADAMTSL-1. Expression of a majority of the investigated ADAMTS members on mRNA level was decreased in aneurysm compared to control aorta. ADAMTS-1 was one of the members that was reduced most. Protein analysis using immunohistochemistry and western blot for localization and expression of ADAMTS-1 revealed that ADAMTS-1 was present predominantly in areas of SMCs and macrophages in aneurysmal aorta and higher expressed in AAA compared to control aortas. The role of ADAMTS-1 in AAA disease was further examined using ADAMTS-1 transgenic/apoE-/- mice with the experimental angiotensin II induced aneurysmal model. Transgenic mice overexpressing ADAMTS-1 showed to be similar to ADAMTS-1 wild type mice pertaining collagen, elastin content and aortic diameter.

CONCLUSION: Several of the ADAMTS members, and especially ADAMTS-1, are down regulated at mRNA level in AAA, due to unknown mechanisms, at the same time ADAMTS-1 protein is induced. The cleavage of its substrates, don't seem to be crucial for the pathogenesis of AAA but rather more important in the development of thoracic aortic aneurysm and atherosclerosis as shown in previous studies.

Place, publisher, year, edition, pages
Public Library of Science, 2017
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:liu:diva-139129 (URN)10.1371/journal.pone.0178729 (DOI)000402611800112 ()28570682 (PubMedID)2-s2.0-85020220425 (Scopus ID)
Note

Funding agencies: Swedish Research Council [2016-02626]; Swedish Heart-Lung Foundation [20160779, 2013-0650]; Ake Wibergs stiftelse [M16-0070]

Available from: 2017-07-03 Created: 2017-07-03 Last updated: 2018-04-18Bibliographically approved
Folkesson, M., Vorkapic, E., Gulbins, E., Japtok, L., Kleuser, B., Welander, M., . . . Wågsäter, D. (2017). Inflammatory cells, ceramides, and expression of proteases in perivascular adipose tissue adjacent to human abdominal aortic aneurysms. Journal of Vascular Surgery, 65(4), 1171
Open this publication in new window or tab >>Inflammatory cells, ceramides, and expression of proteases in perivascular adipose tissue adjacent to human abdominal aortic aneurysms
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2017 (English)In: Journal of Vascular Surgery, ISSN 0741-5214, E-ISSN 1097-6809, Vol. 65, no 4, p. 1171-Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Abdominal aortic aneurysm (AAA) is a deadly irreversible weakening and distension of the abdominal aortic wall. The pathogenesis of AAA remains poorly understood. Investigation into the physical and molecular characteristics of perivascular adipose tissue (PVAT) adjacent to AAA has not been done before and is the purpose of this study.

METHODS AND RESULTS: Human aortae, periaortic PVAT, and fat surrounding peripheral arteries were collected from patients undergoing elective surgical repair of AAA. Control aortas were obtained from recently deceased healthy organ donors with no known arterial disease. Aorta and PVAT was found in AAA to larger extent compared with control aortas. Immunohistochemistry revealed neutrophils, macrophages, mast cells, and T-cells surrounding necrotic adipocytes. Gene expression analysis showed that neutrophils, mast cells, and T-cells were found to be increased in PVAT compared with AAA as well as cathepsin K and S. The concentration of ceramides in PVAT was determined using mass spectrometry and correlated with content of T-cells in the PVAT.

CONCLUSIONS: Our results suggest a role for abnormal necrotic, inflamed, proteolytic adipose tissue to the adjacent aneurysmal aortic wall in ongoing vascular damage.

National Category
Surgery Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:liu:diva-126051 (URN)10.1016/j.jvs.2015.12.056 (DOI)000402625400035 ()26960947 (PubMedID)
Available from: 2016-03-11 Created: 2016-03-11 Last updated: 2017-06-26
Carlsson, A. C., Östgren, C. J., Nyström, F. H., Länne, T., Jennersjö, P., Larsson, A. & Arnlov, J. (2016). Association of soluble tumor necrosis factor receptors 1 and 2 with nephropathy, cardiovascular events, and total mortality in type 2 diabetes. Cardiovascular Diabetology, 15(1), 40
Open this publication in new window or tab >>Association of soluble tumor necrosis factor receptors 1 and 2 with nephropathy, cardiovascular events, and total mortality in type 2 diabetes
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2016 (English)In: Cardiovascular Diabetology, ISSN 1475-2840, E-ISSN 1475-2840, Vol. 15, no 1, p. 40-Article in journal (Refereed) Published
Abstract [en]

Aims/hypothesis: Soluble tumor necrosis factor receptors 1 and 2 (sTNFR1 and sTNFR2) contribute to experimental diabetic kidney disease, a condition with substantially increased cardiovascular risk when present in patients. Therefore, we aimed to explore the levels of sTNFRs, and their association with prevalent kidney disease, incident cardiovascular disease, and risk of mortality independently of baseline kidney function and microalbuminuria in a cohort of patients with type 2 diabetes. In pre-defined secondary analyses we also investigated whether the sTNFRs predict adverse outcome in the absence of diabetic kidney disease. Methods: The CARDIPP study, a cohort study of 607 diabetes patients [mean age 61 years, 44 % women, 45 cardiovascular events (fatal/non-fatal myocardial infarction or stroke) and 44 deaths during follow-up (mean 7.6 years)] was used. Results: Higher sTNFR1 and sTNFR2 were associated with higher odds of prevalent kidney disease [odd ratio (OR) per standard deviation (SD) increase 1.60, 95 % confidence interval (CI) 1.32-1.93, p < 0.001 and OR 1.54, 95 % CI 1.21-1.97, p = 0.001, respectively]. In Cox regression models adjusting for age, sex, glomerular filtration rate and urinary albumin/creatinine ratio, higher sTNFR1 and sTNFR2 predicted incident cardiovascular events [hazard ratio (HR) per SD increase, 1.66, 95 % CI 1.29-2.174, p < 0.001 and HR 1.47, 95 % CI 1.13-1.91, p = 0.004, respectively]. Results were similar in separate models with adjustments for inflammatory markers, HbA1c, or established cardiovascular risk factors, or when participants with diabetic kidney disease at baseline were excluded (p < 0.01 for all). Both sTNFRs were associated with mortality. Conclusions/Interpretations: Higher circulating sTNFR1 and sTNFR2 are associated with diabetic kidney disease, and predicts incident cardiovascular disease and mortality independently of microalbuminuria and kidney function, even in those without kidney disease. Our findings support the clinical utility of sTNFRs as prognostic markers in type 2 diabetes.

Place, publisher, year, edition, pages
BIOMED CENTRAL LTD, 2016
Keyword
Type 2 diabetes; TNF; Laplace regression; Incident cardiovascular disease; Mortality; Inflammation
National Category
Cardiac and Cardiovascular Systems General Practice
Identifiers
urn:nbn:se:liu:diva-126836 (URN)10.1186/s12933-016-0359-8 (DOI)000371581000001 ()26928194 (PubMedID)
Note

Funding Agencies|Swedish Research Council; Swedish Heart-Lung foundation; Thureus foundation; Marianne and Marcus Wallenberg Foundation; Dalarna University; Uppsala University

Available from: 2016-04-05 Created: 2016-04-05 Last updated: 2018-01-10
Wijkman, M., Länne, T., Östgren, C. J. & Nyström, F. H. (2016). Diastolic orthostatic hypertension and cardiovascular prognosis in type 2 diabetes: a prospective cohort study. Cardiovascular Diabetology, 15(83), 1-10
Open this publication in new window or tab >>Diastolic orthostatic hypertension and cardiovascular prognosis in type 2 diabetes: a prospective cohort study
2016 (English)In: Cardiovascular Diabetology, ISSN 1475-2840, E-ISSN 1475-2840, Vol. 15, no 83, p. 1-10Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: In patients with type 2 diabetes, the prognostic impact of an orthostatic rise in blood pressure is not known. Therefore, the aim of this study was to determine the prognostic implications of the diastolic orthostatic blood pressure response in a cohort of patients with type 2 diabetes. We also evaluated associations between different orthostatic blood pressure responses and markers of subclinical cardiovascular organ damage.

METHODS: Office blood pressures were measured in the sitting and in the standing position in 749 patients with type 2 diabetes who participated in the CARDIPP study (Cardiovascular Risk factors in Patients with Diabetes-a Prospective study in Primary care). Diastolic orthostatic hypertension was defined as a rise of diastolic blood pressure ≥10 mmHg and diastolic orthostatic hypotension was defined as a drop of diastolic blood pressure ≥10 mmHg. Recruitment took place between the years 2005-2008, and patients were followed until any of the primary outcome events (cardiovascular death or hospitalization for either myocardial infarction or stroke) occurred or until December 31st, 2014. Measurements of aortic pulse wave velocity and of carotid intima-media thickness were performed at base-line.

RESULTS: Diastolic orthostatic hypertension was found in 140 patients (18.7 %) and was associated with significantly lower risk of cardiovascular events (crude hazard ratio compared with patients with normal systolic and diastolic orthostatic blood pressure response: 0.450, 95 % C.I. 0.206-0.987, P = 0.046). Diastolic orthostatic hypotension was found in 31 patients (4.1 %) and was associated with higher values for aortic pulse wave velocity and carotid intima-media thickness, compared with patients with normal systolic and diastolic orthostatic blood pressure response.

CONCLUSIONS: Diastolic orthostatic hypertension is common in patients with type 2 diabetes, and may be a novel marker for decreased cardiovascular risk in these patients.

Place, publisher, year, edition, pages
BioMed Central, 2016
Keyword
Arterial stiffness, Blood pressure, Cardiovascular risk, Carotid intima-media thickness, Events, Orthostatic hypotension, Type 2 diabetes mellitus
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-129959 (URN)10.1186/s12933-016-0399-0 (DOI)000377852600001 ()27255168 (PubMedID)
Note

Funding agencies: FORSS; Research Council of Southeastern Sweden; King GustafV and Queen Victoria Freemason Foundation, Sweden

Available from: 2016-07-02 Created: 2016-07-02 Last updated: 2017-11-28Bibliographically approved
Folkesson, M., Sadowska, N., Vikingsson, S., Karlsson, M., Carlhäll, C.-J., Länne, T., . . . Jensen, L. (2016). Differences in cardiovascular toxicities associated with cigarette smoking and snuff use revealed using novel zebrafish models. Biology Open, 5(7), 970-978
Open this publication in new window or tab >>Differences in cardiovascular toxicities associated with cigarette smoking and snuff use revealed using novel zebrafish models
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2016 (English)In: Biology Open, ISSN 2046-6390, Vol. 5, no 7, p. 970-978Article in journal (Refereed) Published
Abstract [en]

Tobacco use is strongly associated with cardiovascular disease and the only avoidable risk factor associated with development of aortic aneurysm. While smoking is the most common form of tobacco use, snuff and other oral tobacco products are gaining popularity, but research on potentially toxic effects of oral tobacco use has not kept pace with the increase in its use. Here, we demonstrate that cigarette smoke and snuff extracts are highly toxic to developing zebrafish embryos. Exposure to such extracts led to a palette of toxic effects including early embryonic mortality, developmental delay, cerebral hemorrhages, defects in lymphatics development and ventricular function, and aneurysm development. Both cigarette smoke and snuff were more toxic than pure nicotine, indicating that other compounds in these products are also associated with toxicity. While some toxicities were found following exposure to both types of tobacco product, other toxicities, including developmental delay and aneurysm development, were specifically observed in the snuff extract group, whereas cerebral hemorrhages were only found in the group exposed to cigarette smoke extract. These findings deepen our understanding of the pathogenic effects of cigarette smoking and snuff use on the cardiovascular system and illustrate the benefits of using zebrafish to study mechanisms involved in aneurysm development.

Place, publisher, year, edition, pages
Company of Biologists, 2016
Keyword
Aneurysm; Aorta; Cardiovascular; Snuff; Tobacco; Zebrafish
National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:liu:diva-130706 (URN)10.1242/bio.018812 (DOI)000380569100010 ()27334697 (PubMedID)
Note

The Jensen laboratory is supported by grants from Svenska Sallskapet for Medicinsk Forskning [grant F14-0021], Linkopings Universitet, Eva och Oscar Ahrens Stiftelse, Ollie och Elof Ericssons Stiftelse, Carmen och Bertil Ragners Stiftelse, Gosta Fraenkels Stiftelse, Ake Wibergs Stiftelse, Lions Forskningsfond, Karin Sandbergs Stiftelse, Cancerfonden, Karolinska Institutet's Stiftelser och Fonder and Vetenskapsradet [grant 2015-06271].

Available from: 2016-08-21 Created: 2016-08-21 Last updated: 2018-03-19
Good, E., Länne, T., Wilhelm, E., Perk, J., Jaarsma, T. & de Muinck, E. (2016). High-grade carotid artery stenosis: A forgotten area in cardiovascular risk management. European Journal of Preventive Cardiology, 23(13), 1453-1460
Open this publication in new window or tab >>High-grade carotid artery stenosis: A forgotten area in cardiovascular risk management
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2016 (English)In: European Journal of Preventive Cardiology, ISSN 2047-4873, E-ISSN 2047-4881, Vol. 23, no 13, p. 1453-1460Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Patients with high-grade (≥70%) carotid artery stenosis (CAS) rank in the highest risk category for future cardiovascular (CV) events, but the quality of cardiovascular risk management in this patient group is unknown.

DESIGN: Cross-sectional retrospective study.

METHODS: Data were collected for all patients diagnosed with high-grade CAS in Östergötland county, Sweden between 1 January 2009 and 31 July 2012 regarding the quality of cardiovascular risk management, co-morbidity and outcomes during the 2-year follow-up period after a diagnosis of CAS with a carotid ultrasound scan. Patients were included regardless of whether they underwent carotid endarterectomy (CEA).

RESULTS: A total of 393 patients with CAS were included in the study; 133 (33.8%) underwent CEA and 260 (66.2%) were assigned to a conservative management (CM) group. In both groups of patients the prescription of platelet inhibitors, statins and antihypertensive drugs increased significantly (p < 0.001) after diagnosis. However treatment targets were not met in the majority of patients and the low-density lipoprotein level was on target in only 13.5% of patients. During follow-up, low-density lipoprotein levels were not measured in 19.8% of patients who underwent CEA and 44.2% of patients in the CM group (p < 0.001); HbA1c was not measured in 24.4% of patients with diabetes in the CEA group and in 18.8% of patients in the CM group (p = 0.560). There was no documentation of counselling on diet, exercise, smoking cessation or adherence to medication. The combined clinical event rate (all-cause mortality, cardiovascular mortality and non-fatal cardiovascular events) was high in both groups (CEA 36.8% and CM 36.9%; p = 1.00) with no difference in the occurrence of ipsilateral ischaemic stroke.

CONCLUSIONS: The clinical event rate was high in patients with high-grade CAS and the management of cardiovascular risk was deficient in all aspects.

Place, publisher, year, edition, pages
Sage Publications, 2016
Keyword
High-grade carotid stenosis, atherosclerosis, cardiovascular disease, cardiovascular risk management, secondary prevention
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-129961 (URN)10.1177/2047487316632629 (DOI)000382655100013 ()26879568 (PubMedID)
Note

Funding agencies. Linkoping University Hospital [LIO-417951]

Available from: 2016-07-02 Created: 2016-07-02 Last updated: 2017-11-28Bibliographically approved
Skoog, J., Lindenberger, M., Ekman, M., Holmberg, B., Zachrisson, H. & Länne, T. (2016). Reduced venous compliance: an important determinant for orthostatic intolerance in women with vasovagal syncope. American Journal of Physiology. Regulatory Integrative and Comparative Physiology, 310(3), R253-R261
Open this publication in new window or tab >>Reduced venous compliance: an important determinant for orthostatic intolerance in women with vasovagal syncope
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2016 (English)In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 310, no 3, p. R253-R261Article in journal (Refereed) Published
Abstract [en]

The influence of lower limb venous compliance on orthostatic vasovagal syncope (VVS) is uncertain. The most widespread technique to calculate venous compliance uses a nonphysiological quadratic regression equation. Our aim was therefore to construct a physiologically derived venous wall model (VWM) for calculation of calf venous compliance and to determine the effect of venous compliance on tolerance to maximal lower body negative pressure (LBNP). Venous occlusion plethysmography was used to study calf volume changes in 15 women with VVS (25.5 +/- 1.3 yr of age) and 15 controls (22.8 +/- 0.8 yr of age). The fit of the VWM and the regression equation to the experimentally induced pressure-volume curve was examined. Venous compliance was calculated as the derivative of the modeled pressure-volume relationship. Graded LBNP to presyncope was used to determine the LBNP tolerance index (LTI). The VWM displayed a better fit to the experimentally induced pressure-volume curve (P &lt; 0.0001). Calf blood pooling was similar in the groups and was not correlated to the LTI (r = 0.204, P = 0.30). Venous compliance was significantly reduced at low venous pressures in women with VVS (P = 0.042) and correlated to the LTI (r = 0.459, P = 0.014) in the low pressure range. No correlation was found between venous compliance at high venous pressures and the LTI. In conclusion, the new VWM accurately adopted the curvilinear pressure-volume curve, providing a valid characterization of venous compliance. Reduced venous compliance at low venous pressures may adversely affect mobilization of peripheral venous blood to the central circulation during hypovolemic circulatory stress in women with VVS.

Place, publisher, year, edition, pages
AMER PHYSIOLOGICAL SOC, 2016
Keyword
vasovagal syncope; orthostatic intolerance; venous compliance; venous capacitance
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-125296 (URN)10.1152/ajpregu.00362.2015 (DOI)000369058900005 ()26561647 (PubMedID)
Note

Funding Agencies|Futurum-The Academy of Health Care; Jonkoping County Council; Medical Research Council of Southeast Sweden; Heart and Lung Foundation

Available from: 2016-02-24 Created: 2016-02-19 Last updated: 2017-04-26
Skoog, J., Zachrisson, H., Länne, T. & Lindenberger, M. (2016). Slower Lower Limb Blood Pooling Increases Orthostatic Tolerance in Women with Vasovagal Syncope. Frontiers in Physiology, 7(232)
Open this publication in new window or tab >>Slower Lower Limb Blood Pooling Increases Orthostatic Tolerance in Women with Vasovagal Syncope
2016 (English)In: Frontiers in Physiology, ISSN 1664-042X, E-ISSN 1664-042X, Vol. 7, no 232Article in journal (Refereed) Published
Abstract [en]

Background and Aim: Slower lower limb blood pooling and associated blunted sympathetic activation has been detected in healthy women prone to orthostatic syncope. Whether these findings are true also for patients with vasovagal syncope (WS) is unknown. The aim was to investigate initial blood pooling time (pooling(time), time to 50% of total blood pooling) together with hemodynamic responses and orthostatic tolerance during lower body negative pressure (LBNP) in WS and healthy controls. Methods and Results: Fourteen WS women (25.7 +/- 1.3 years) and 15 healthy women (22.8 +/- 0.8 years) were subjected to single-step and graded LBNP to pre-syncope. Lower limb blood pooling (ml 100 ml(-1)), poolingtime (s), hemodynamic responses and LBNP-tolerance were evaluated. LBNP induced comparable lower limb blood pooling in both groups (controls, 3.1 +/- 0.3; WS, 2.9 +/- 0.3 ml 100 ml(-1), P = 0.70). In controls, shorter pooling(time) correlated to higher LBNP-tolerance (r = -0.550, P amp;lt; 0.05) as well as better maintained stroke volume (r =-0.698, P amp;lt; 0.01) and cardiac output (r = -0.563, P amp;lt; 0.05). In contrast, shorter poolingtime correlated to lower LBNP-tolerance in VVS (r = 0.821, P amp;lt; 0.001) and larger decline in stroke volume (r = 0.611, P 0.05). Furthermore, in controls, shorter poolingtime correlated to baroreflex-mediated hemodynamic changes during LBNP, e.g., increased vasoconstriction (P amp;lt; 0.001). In VVS, poolingtime was not correlated with LBNP-induced baroreceptor unloading, but rather highly correlated to resting calf blood flow (P amp;lt; 0.001). Conclusions: Shorter poolingtime seems to elicit greater sympathetic activation with a concomitant higher orthostatic tolerance in healthy women. The contrasting findings in AS indicate a deteriorated vascular sympathetic control suggesting well-defined differences already in the initial responses during orthostatic stress.

Place, publisher, year, edition, pages
FRONTIERS MEDIA SA, 2016
Keyword
syncope; blood pooling; orthostatic intolerance; hemodynamics; baroreceptors; veins; sympathetic nervous system
National Category
Physiology
Identifiers
urn:nbn:se:liu:diva-130129 (URN)10.3389/fphys.2016.00232 (DOI)000377761400001 ()27378941 (PubMedID)
Note

Funding Agencies|Futurum-the Academy of Health Care, Jonkoping County Council; Medical Research Council of Southeast Sweden; Heart and Lung Foundation; County Council of Ostergotland

Available from: 2016-07-12 Created: 2016-07-11 Last updated: 2018-01-10
Carlsson, A. C., Östgren, C. J., Länne, T., Larsson, A., Nyström, F. H. & Ärnlöv, J. (2016). The association between endostatin and kidney disease and mortality in patients with type 2 diabetes. Diabetes & Metabolism, 42(5), 351-357
Open this publication in new window or tab >>The association between endostatin and kidney disease and mortality in patients with type 2 diabetes
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2016 (English)In: Diabetes & Metabolism, ISSN 1262-3636, E-ISSN 1878-1780, Vol. 42, no 5, p. 351-357Article in journal (Refereed) Published
Abstract [en]

AIM: Circulating endostatin, a biologically active derivate of collagen XVIII, is considered to be a marker of kidney disease and a risk factor for its related mortality. However, less is known of the role of endostatin in diabetes and the development of diabetic nephropathy. For this reason, our study investigated the associations between circulating endostatin and the prevalence and progression of kidney disease, and its mortality risk in patients with type 2 diabetes (T2D).

METHODS: This was a cohort study of 607 patients with T2D (mean age: 61 years, 44% women). Estimated glomerular filtration rate (eGFR), calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) creatinine equation, was used to assess the patients' kidney function decline and mortality.

RESULTS: Of the total study cohort, 20 patients declined by ≥20% in eGFR over 4 years, and 44 died during the follow-up (mean duration: 6.7 years). At baseline, participants with diabetic nephropathy (defined as eGFR<60mL/min/1.73m(2)) and/or microalbuminuria [defined as a urinary albumin-to-creatinine ratio (ACR)>3g/mol] had higher median levels of endostatin than those without nephropathy (62.7μg/L vs 57.4μg/L, respectively; P=0.031). In longitudinal analyses adjusted for age, gender, baseline eGFR and ACR, higher endostatin levels were associated with a higher risk of decline (≥20% in eGFR, OR per 1 SD increase: 1.73, 95% CI: 1.13-2.65) and a higher risk of mortality (HR per 1 SD increase: 1.57, 95% CI: 1.19-2.07).

CONCLUSION: In patients with T2D, circulating endostatin levels can predict the progression of kidney disease and mortality independently of established kidney disease markers. The clinical usefulness of endostatin as a risk marker in such patients merits further studies.

Place, publisher, year, edition, pages
Elsevier, 2016
Keyword
Albumin-to-creatinine ratio, Angiogenesis, Chronic kidney disease, Community, Extracellular matrix remodeling, NIDDM
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-129960 (URN)10.1016/j.diabet.2016.03.006 (DOI)000392262700006 ()27080454 (PubMedID)
Note

Funding agencies: Swedish Research Council; Swedish Heart-Lung Foundation; Marianne and Marcus Wallenberg Foundation; European Union [634869]

Available from: 2016-07-02 Created: 2016-07-02 Last updated: 2017-11-28Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-9095-403x

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