Skip header and navigation

Refine By

21 records – page 1 of 3.

Age or waist as determinant of insulin action?

https://arctichealth.org/en/permalink/ahliterature184435
Source
Metabolism. 2003 Jul;52(7):850-7
Publication Type
Article
Date
Jul-2003
Author
Bente Bryhni
Trond G Jenssen
Kjell Olafsen
Jorunn H Eikrem
Author Affiliation
Department of Clinical Medicine, University of Tromsø, Norway.
Source
Metabolism. 2003 Jul;52(7):850-7
Date
Jul-2003
Language
English
Publication Type
Article
Keywords
Abdomen
Adipose Tissue
Adult
Aged
Aging
Blood Glucose - metabolism
Body Composition
Body constitution
Body mass index
Fatty Acids, Nonesterified - blood
Glucose Clamp Technique
Glucose Tolerance Test
Humans
Insulin - blood - pharmacology
Male
Oxygen consumption
Regression Analysis
Triglycerides - blood
Abstract
Several studies have shown that insulin action deteriorates with age, possibly mediated through accumulation of abdominal fat. We determined peripheral insulin action in elderly and younger men who had participated in a large population study (the Tromsø Study). To 15 elderly participants aged 71 to 77 years, we individually matched 15 younger participants aged 31 to 33 years (Y1) by body mass index (BMI). A second young group (Y2) comprised 15 participants also aged 31 to 33 years, but with BMI representative of this age group in the population study. All underwent hyperinsulinemic euglycemic clamps (0.4 mU/kg/min), oral glucose tolerance tests, and determinations of Vo2max. Insulin sensitivity index (ISI=glucose disposal per kg fat-free mass [FFM] divided by steady-state insulin concentration) did not differ between the elderly and Y1, but was higher in Y2 (0.10+/-0.01, 0.12+/-0.01, and 0.17+/-0.02, P=.0011 by analysis of variance [ANOVA]). Adjustment by waist circumferences (analysis of covariance [ANCOVA]) abolished this difference. In univariate analysis of pooled data, ISI correlated negatively to body fat indices, serum triglycerides, and free fatty acids (FFA), and positively to Vo2max. In multiple regression analysis, waist circumference and triglycerides were the only independent predictors of insulin sensitivity, whereas age had no impact. The results confirm that the decline in insulin action seen in elderly people is related to increased abdominal fat rather than aging per se.
PubMed ID
12870160 View in PubMed
Less detail

The Association Between Adiponectin, Serum Uric Acid and Urinary Markers of Renal Damage in the General Population: Cross-Sectional Data from the Tromsø Study.

https://arctichealth.org/en/permalink/ahliterature276069
Source
Kidney Blood Press Res. 2016 Sep 14;41(5):623-634
Publication Type
Article
Date
Sep-14-2016
Author
Marit D Solbu
Jon V Norvik
Hilde M Storhaug
Bjørn O Eriksen
Toralf Melsom
Anne Elise Eggen
Svetlana N Zykova
Jens B Kronborg
Trond G Jenssen
Source
Kidney Blood Press Res. 2016 Sep 14;41(5):623-634
Date
Sep-14-2016
Language
English
Publication Type
Article
Abstract
Uric acid may cause renal damage, whereas adiponectin in some studies has been reported to have renoprotective properties. The renoprotective role of adiponectin under the influence of hyperuricemia has not been explored. We assessed the cross-sectional association between adiponectin, serum uric acid (SUA) and urinary biomarkers of glomerular and tubular damage (albumin-creatinine ratio [ACR] and N-acetyl-ß-D-glucosaminidase-creatinine ratio [NAG-CR]) in a large cohort from a general population.
Three urine specimens from 7062 persons, participating in the Tromsø Study, were collected. The adjusted associations between adiponectin and SUA as independent variables, and ACR =1.13 mg/mmol (albuminuria) and the upper gender specific 15 percentile of NAG-CR (high NAG-CR) as dependent variables, were assessed.
Mean (standard deviation) age of the participants was 63.5 (9.2) years. Adiponectin was positively associated with albuminuria and high NAG-CR. SUA was associated with albuminuria (odds ratio [OR] 1.13; 95% Confidence Interval [CI] 1.05-1.21 per 59 µmol/L increase), but not with NAG-CR. There were no statistically significant interactions between SUA and adiponectin.
Unexpectedly, adiponectin was positively associated with both urinary markers of renal damage. SUA was positively associated with albuminuria only. SUA and adiponectin added little beyond traditional cardiovascular risk factors to predict renal damage and did not interact in their associations with the urinary biomarkers. Longitudinal studies are needed before firm conclusions can be made.
PubMed ID
27622764 View in PubMed
Less detail

Blood pressure and age-related GFR decline in the general population.

https://arctichealth.org/en/permalink/ahliterature289947
Source
BMC Nephrol. 2017 Feb 28; 18(1):77
Publication Type
Journal Article
Date
Feb-28-2017
Author
Bjørn O Eriksen
Vidar T N Stefansson
Trond G Jenssen
Ulla D Mathisen
Jørgen Schei
Marit D Solbu
Tom Wilsgaard
Toralf Melsom
Author Affiliation
Metabolic and Renal Research Group, UiT The Arctic University of Norway, Tromsø, Norway. bjorn.odvar.eriksen@unn.no.
Source
BMC Nephrol. 2017 Feb 28; 18(1):77
Date
Feb-28-2017
Language
English
Publication Type
Journal Article
Keywords
Aging
Computer simulation
Female
Glomerular Filtration Rate
Humans
Hypertension - complications - epidemiology - physiopathology
Kidney - physiopathology
Male
Middle Aged
Models, Biological
Norway - epidemiology
Reference Values
Renal Insufficiency, Chronic - complications - epidemiology - physiopathology
Reproducibility of Results
Sensitivity and specificity
Abstract
Hypertension is one of the most important causes of end-stage renal disease, but it is unclear whether elevated blood pressure (BP) also accelerates the gradual decline in the glomerular filtration rate (GFR) seen in the general population with increasing age. The reason may be that most studies have considered only baseline BP and not the effects of changes in BP, antihypertensive treatment and other determinants of GFR during follow-up. Additionally, the use of GFR estimated from creatinine or cystatin C instead of measurements of GFR may have biased the results because of influence from non-GFR related confounders. We studied the relationship between BP and GFR decline using time-varying variables in a cohort representative of the general population using measurements of GFR as iohexol clearance.
We included 1594 subjects aged 50 to 62 years without baseline diabetes, kidney-, or cardiovascular disease in the Renal Iohexol-clearance Survey in Tromsø 6 (RENIS-T6). GFR, BP, antihypertensive medication and all adjustment variables were ascertained at baseline, and at follow-up after a median observation time of 5.6 years in 1299 persons (81%). The relationship between GFR decline and BP was analyzed in linear mixed models.
The mean (standard deviation) GFR decline rate was 0.95 (2.23) mL/min/year. The percentage of persons with hypertension (systolic BP?=?140 mmHg, diastolic BP?=?90 mmHg or antihypertensive medication) increased from 42 to 52% between baseline and follow-up. In multivariable adjusted linear mixed models using time-varying independent variables measured at baseline and follow-up, higher systolic and diastolic BP were associated with slower GFR decline rates by 0.10 and 0.20 mL/min/year/10 mmHg, respectively (p?
Notes
Cites: Am J Kidney Dis. 2014 Sep;64(3):411-24 PMID 24840668
Cites: J Am Soc Nephrol. 2015 Jun;26(6):1261-7 PMID 25525178
Cites: J Hum Hypertens. 2001 Feb;15(2):99-106 PMID 11317188
Cites: N Engl J Med. 2012 Jul 5;367(1):20-9 PMID 22762315
Cites: Circulation. 2016 Feb 9;133(6):584-91 PMID 26762524
Cites: Clin Biochem. 1991 Jun;24(3):261-4 PMID 1908359
Cites: Contrib Nephrol. 1996;119:98-102 PMID 8783598
Cites: Scand J Urol Nephrol. 1995 Jun;29(2):135-9 PMID 7569789
Cites: N Engl J Med. 1994 Mar 31;330(13):877-84 PMID 8114857
Cites: Arch Intern Med. 2000 Mar 13;160(5):685-93 PMID 10724055
Cites: J Am Soc Nephrol. 2003 Nov;14(11):2934-41 PMID 14569104
Cites: Diabetes Care. 2003 Jan;26(1):156-62 PMID 12502673
Cites: J Hypertens. 2015 Jan;33(1):136-43 PMID 25255396
Cites: Clin J Am Soc Nephrol. 2014 Nov 7;9(11):1892-902 PMID 25318758
Cites: Nephrol Dial Transplant. 2012 May;27(5):1821-5 PMID 22140135
Cites: J Am Soc Nephrol. 2006 Mar;17(3):846-53 PMID 16452492
Cites: Nephrol Dial Transplant. 2008 Apr;23(4):1265-73 PMID 18039642
Cites: J Hypertens. 2012 Mar;30(3):497-504 PMID 22278141
Cites: Lancet. 2016 Jan 30;387(10017):435-43 PMID 26559744
Cites: N Engl J Med. 1996 Jan 4;334(1):13-8 PMID 7494564
Cites: JAMA. 2004 Feb 18;291(7):844-50 PMID 14970063
Cites: Am J Kidney Dis. 2012 Jan;59(1):41-9 PMID 22000727
Cites: J Hypertens. 1995 Mar;13(3):357-65 PMID 7622857
Cites: Nephrol Dial Transplant. 2008 Apr;23(4):1246-51 PMID 17984108
Cites: Hypertension. 2000 Mar;35(3):822-6 PMID 10720601
Cites: Kidney Int. 2007 Jan;71(2):159-66 PMID 17136030
Cites: Kidney Int. 2016 Aug;90(2):404-10 PMID 27188503
Cites: Am J Hypertens. 2013 Aug;26(8):1037-44 PMID 23709568
Cites: Am J Kidney Dis. 2015 Jul;66(1 Suppl 1):Svii, S1-305 PMID 26111994
Cites: Am J Hypertens. 2012 Jan;25(1):126-32 PMID 21993366
Cites: BMC Nephrol. 2014 Mar 14;15:45 PMID 24628838
Cites: J Am Soc Nephrol. 2009 Nov;20(11):2305-13 PMID 19833901
Cites: Kidney Int. 1996 Jun;49(6):1774-7 PMID 8743495
Cites: Nephrol Dial Transplant. 2010 Jun;25(6):1846-53 PMID 20054026
Cites: Am J Physiol Renal Physiol. 2015 Feb 1;308(3):F167-78 PMID 25377913
Cites: J Am Soc Nephrol. 2011 May;22(5):927-37 PMID 21454717
Cites: Am J Hypertens. 2012 Sep;25(9):1011-6 PMID 22673015
Cites: J Hypertens. 2013 Dec;31(12):2410-7 PMID 24029869
Cites: Am J Kidney Dis. 2009 Oct;54(4):638-46 PMID 19515474
Cites: Kidney Int. 2004 Apr;65(4):1416-21 PMID 15086483
Cites: JAMA. 1993 Jan 27;269(4):488-93 PMID 8419668
Cites: Kidney Int. 2013 Jun;83(6):1169-76 PMID 23423253
Cites: Arch Intern Med. 2005 Apr 25;165(8):923-8 PMID 15851645
Cites: J Clin Epidemiol. 2013 Sep;66(9):1022-8 PMID 23790725
Cites: Kidney Int. 1984 Dec;26(6):861-8 PMID 6533397
Cites: Nephrol Dial Transplant. 1998 May;13(5):1176-82 PMID 9623550
Cites: JAMA. 2002 Nov 20;288(19):2421-31 PMID 12435255
Cites: Nephron. 2015;131(3):175-84 PMID 26426198
Cites: Nephrol Dial Transplant. 2008 Sep;23(9):2818-26 PMID 18400822
Cites: N Engl J Med. 2002 Oct 17;347(16):1256-61 PMID 12393824
Cites: N Engl J Med. 2003 Jan 9;348(2):101-8 PMID 12519920
Cites: Hypertension. 2000 Apr;35(4):952-7 PMID 10775568
Cites: Am J Kidney Dis. 2010 Jan;55(1):31-41 PMID 19932544
Cites: Am J Kidney Dis. 2016 Jan;67(1):89-97 PMID 26475392
Cites: N Engl J Med. 2015 Nov 26;373(22):2103-16 PMID 26551272
Cites: Am J Hypertens. 2015 Sep;28(9):1150-6 PMID 25673040
Cites: Atherosclerosis. 2008 Dec;201(2):398-406 PMID 18405901
Cites: Hypertension. 2003 Dec;42(6):1144-9 PMID 14597644
Cites: Nephrol Dial Transplant. 2015 Aug;30(8):1237-43 PMID 25326471
Cites: Kidney Int. 2010 Dec;78(12):1305-11 PMID 20844470
PubMed ID
28245797 View in PubMed
Less detail

Blood pressure and age-related GFR decline in the general population.

https://arctichealth.org/en/permalink/ahliterature280506
Source
BMC Nephrol. 2017 Feb 28;18(1):77
Publication Type
Article
Date
Feb-28-2017
Author
Bjørn O Eriksen
Vidar T N Stefansson
Trond G Jenssen
Ulla D Mathisen
Jørgen Schei
Marit D Solbu
Tom Wilsgaard
Toralf Melsom
Source
BMC Nephrol. 2017 Feb 28;18(1):77
Date
Feb-28-2017
Language
English
Publication Type
Article
Abstract
Hypertension is one of the most important causes of end-stage renal disease, but it is unclear whether elevated blood pressure (BP) also accelerates the gradual decline in the glomerular filtration rate (GFR) seen in the general population with increasing age. The reason may be that most studies have considered only baseline BP and not the effects of changes in BP, antihypertensive treatment and other determinants of GFR during follow-up. Additionally, the use of GFR estimated from creatinine or cystatin C instead of measurements of GFR may have biased the results because of influence from non-GFR related confounders. We studied the relationship between BP and GFR decline using time-varying variables in a cohort representative of the general population using measurements of GFR as iohexol clearance.
We included 1594 subjects aged 50 to 62 years without baseline diabetes, kidney-, or cardiovascular disease in the Renal Iohexol-clearance Survey in Tromsø 6 (RENIS-T6). GFR, BP, antihypertensive medication and all adjustment variables were ascertained at baseline, and at follow-up after a median observation time of 5.6 years in 1299 persons (81%). The relationship between GFR decline and BP was analyzed in linear mixed models.
The mean (standard deviation) GFR decline rate was 0.95 (2.23) mL/min/year. The percentage of persons with hypertension (systolic BP?=?140 mmHg, diastolic BP?=?90 mmHg or antihypertensive medication) increased from 42 to 52% between baseline and follow-up. In multivariable adjusted linear mixed models using time-varying independent variables measured at baseline and follow-up, higher systolic and diastolic BP were associated with slower GFR decline rates by 0.10 and 0.20 mL/min/year/10 mmHg, respectively (p?
Notes
Cites: Am J Kidney Dis. 2014 Sep;64(3):411-2424840668
Cites: J Am Soc Nephrol. 2015 Jun;26(6):1261-725525178
Cites: J Hum Hypertens. 2001 Feb;15(2):99-10611317188
Cites: N Engl J Med. 2012 Jul 5;367(1):20-922762315
Cites: Circulation. 2016 Feb 9;133(6):584-9126762524
Cites: Clin Biochem. 1991 Jun;24(3):261-41908359
Cites: Contrib Nephrol. 1996;119:98-1028783598
Cites: Scand J Urol Nephrol. 1995 Jun;29(2):135-97569789
Cites: N Engl J Med. 1994 Mar 31;330(13):877-848114857
Cites: Arch Intern Med. 2000 Mar 13;160(5):685-9310724055
Cites: J Am Soc Nephrol. 2003 Nov;14(11):2934-4114569104
Cites: Diabetes Care. 2003 Jan;26(1):156-6212502673
Cites: J Hypertens. 2015 Jan;33(1):136-4325255396
Cites: Clin J Am Soc Nephrol. 2014 Nov 7;9(11):1892-90225318758
Cites: Nephrol Dial Transplant. 2012 May;27(5):1821-522140135
Cites: J Am Soc Nephrol. 2006 Mar;17(3):846-5316452492
Cites: Nephrol Dial Transplant. 2008 Apr;23(4):1265-7318039642
Cites: J Hypertens. 2012 Mar;30(3):497-50422278141
Cites: Lancet. 2016 Jan 30;387(10017):435-4326559744
Cites: N Engl J Med. 1996 Jan 4;334(1):13-87494564
Cites: JAMA. 2004 Feb 18;291(7):844-5014970063
Cites: Am J Kidney Dis. 2012 Jan;59(1):41-922000727
Cites: J Hypertens. 1995 Mar;13(3):357-657622857
Cites: Nephrol Dial Transplant. 2008 Apr;23(4):1246-5117984108
Cites: Hypertension. 2000 Mar;35(3):822-610720601
Cites: Kidney Int. 2007 Jan;71(2):159-6617136030
Cites: Kidney Int. 2016 Aug;90(2):404-1027188503
Cites: Am J Hypertens. 2013 Aug;26(8):1037-4423709568
Cites: Am J Kidney Dis. 2015 Jul;66(1 Suppl 1):Svii, S1-30526111994
Cites: Am J Hypertens. 2012 Jan;25(1):126-3221993366
Cites: BMC Nephrol. 2014 Mar 14;15:4524628838
Cites: J Am Soc Nephrol. 2009 Nov;20(11):2305-1319833901
Cites: Kidney Int. 1996 Jun;49(6):1774-78743495
Cites: Nephrol Dial Transplant. 2010 Jun;25(6):1846-5320054026
Cites: Am J Physiol Renal Physiol. 2015 Feb 1;308(3):F167-7825377913
Cites: J Am Soc Nephrol. 2011 May;22(5):927-3721454717
Cites: Am J Hypertens. 2012 Sep;25(9):1011-622673015
Cites: J Hypertens. 2013 Dec;31(12):2410-724029869
Cites: Am J Kidney Dis. 2009 Oct;54(4):638-4619515474
Cites: Kidney Int. 2004 Apr;65(4):1416-2115086483
Cites: JAMA. 1993 Jan 27;269(4):488-938419668
Cites: Kidney Int. 2013 Jun;83(6):1169-7623423253
Cites: Arch Intern Med. 2005 Apr 25;165(8):923-815851645
Cites: J Clin Epidemiol. 2013 Sep;66(9):1022-823790725
Cites: Kidney Int. 1984 Dec;26(6):861-86533397
Cites: Nephrol Dial Transplant. 1998 May;13(5):1176-829623550
Cites: JAMA. 2002 Nov 20;288(19):2421-3112435255
Cites: Nephron. 2015;131(3):175-8426426198
Cites: Nephrol Dial Transplant. 2008 Sep;23(9):2818-2618400822
Cites: N Engl J Med. 2002 Oct 17;347(16):1256-6112393824
Cites: N Engl J Med. 2003 Jan 9;348(2):101-812519920
Cites: Hypertension. 2000 Apr;35(4):952-710775568
Cites: Am J Kidney Dis. 2010 Jan;55(1):31-4119932544
Cites: Am J Kidney Dis. 2016 Jan;67(1):89-9726475392
Cites: N Engl J Med. 2015 Nov 26;373(22):2103-1626551272
Cites: Am J Hypertens. 2015 Sep;28(9):1150-625673040
Cites: Atherosclerosis. 2008 Dec;201(2):398-40618405901
Cites: Hypertension. 2003 Dec;42(6):1144-914597644
Cites: Nephrol Dial Transplant. 2015 Aug;30(8):1237-4325326471
Cites: Kidney Int. 2010 Dec;78(12):1305-1120844470
PubMed ID
28245797 View in PubMed
Less detail

Cardiovascular risk-factors predict progression of urinary albumin-excretion in a general, non-diabetic population: a gender-specific follow-up study.

https://arctichealth.org/en/permalink/ahliterature157774
Source
Atherosclerosis. 2008 Dec;201(2):398-406
Publication Type
Article
Date
Dec-2008
Author
Marit D Solbu
Jens Kronborg
Bjørn O Eriksen
Trond G Jenssen
Ingrid Toft
Author Affiliation
Department of Nephrology, University Hospital of North Norway, Tromsø, Norway. Marit.Solbu@fagmed.uit.no
Source
Atherosclerosis. 2008 Dec;201(2):398-406
Date
Dec-2008
Language
English
Publication Type
Article
Keywords
Adult
Aged
Albuminuria - metabolism - pathology
Antihypertensive Agents - pharmacology
Cardiovascular Diseases - metabolism - pathology - urine
Female
Follow-Up Studies
Glomerular Filtration Rate
Humans
Hypertension - drug therapy
Male
Middle Aged
Risk factors
Sex Factors
Waist Circumference
Abstract
Increased urinary albumin-excretion (UAE) predicts cardiovascular events and clusters with the metabolic syndrome. The aim of this population-based, prospective study was to assess the relationship between baseline and longitudinal changes in cardiovascular risk-factors and 7 years' increase in UAE. Three thousand and four hundred non-diabetic participants (1838 men, 1562 women) of the Tromsø studies in 1994/1995 and 2001/2002 were included. In each survey, first-void spot-urine-samples were collected, and albumin-creatinine ratio (ACR) was calculated. Change in ACR (DeltaACR) was dichotomized into upper vs. the three lower quartiles. Median UAE in the population did not increase during follow-up. Baseline predictors for DeltaACR in the upper quartile were: age (OR 1.32 per 5 years, 95% CI 1.22-1.43), HbA1c (OR 1.43 per %, 95% CI 1.08-1.91) and waist circumference (OR 1.11 per 5 cm, 95% CI 1.04-1.19) in men, and age (OR 1.14 per 5 years, 95% CI 1.04-1.25) and current smoking (OR 1.71, 95% CI 1.27-2.30) in women. Systolic blood pressure and estimated glomerular filtration rate were predictors without gender-specificity. Clustering of three or more metabolic traits did not predict ACR increase independently. Protective factors against ACR increase were initiation of antihypertensive treatment in women (OR 0.59, 95% CI 0.39-0.87) and hard physical activity in men (OR 0.70, 95% CI 0.51-0.96). In summary, cardiovascular risk-factors at baseline predicted ACR increase, but initiation of antihypertensive therapy (women) and physical activity (men) seemed to protect from ACR increase during follow-up. Endpoint-data are needed to explore the clinical significance of low-grade UAE increase.
PubMed ID
18405901 View in PubMed
Less detail

Cost and clinical outcome of islet transplantation in Norway 2010-2015.

https://arctichealth.org/en/permalink/ahliterature289965
Source
Clin Transplant. 2017 01; 31(1):
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
01-2017
Author
Simen W Schive
Aksel Foss
Afaf Sahraoui
Kristine Kloster-Jensen
Geir Hafsahl
Gunnar Kvalheim
Torbjørn Lundgren
Bengt von Zur-Mühlen
Marie Felldin
Ehab Rafael
Marko Lempinen
Olle Korsgren
Trond G Jenssen
Vinod Mishra
Hanne Scholz
Author Affiliation
Department of Transplant Medicine, Cancer Institute, Oslo University Hospital, Oslo, Norway.
Source
Clin Transplant. 2017 01; 31(1):
Date
01-2017
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Adult
Diabetes Mellitus, Type 1 - economics - surgery
Female
Follow-Up Studies
Graft Rejection - economics - epidemiology
Graft Survival
Humans
Incidence
Islets of Langerhans Transplantation - economics - methods
Male
Middle Aged
Norway - epidemiology
Postoperative Complications - economics - epidemiology
Retrospective Studies
Time Factors
Treatment Outcome
Abstract
Islet transplantation is a minimally invasive ß-cell replacement strategy. Islet transplantation is a reimbursed treatment in Norway. Here, we summarize the cost and clinical outcome of 31 islet transplantations performed at Oslo University Hospital (OUS) from January 2010 to June 2015. Patients were retrospectively divided into three groups. Thirteen patients received either one or two islet transplantation alone (ITA), while five patients received islet transplantation after previous solid organ transplantation. For the group receiving 2 ITA, Kaplan-Meier estimates show an insulin independence of 20% more than 4 years after their last transplantation. An estimated 70% maintain at least partial graft function, defined as fasting C-peptide >0.1 nmol L-1 , and 47% maintain a HbA1c below 6.5% or 2 percent points lower than before ITA. For all groups combined, we estimate that 44% of the patients have a 50% reduction in insulin requirement 4 years after the initial islet transplantation. The average cost for an islet transplantation procedure was 347 297±60 588 NOK, or 35 424±6182 EUR, of which isolation expenses represent 34%. We hereby add to the common pool of growing experience with islet transplantation and also describe the cost of the treatment at our center.
PubMed ID
27862341 View in PubMed
Less detail

Cross-sectional analysis of nutrition and serum uric acid in two Caucasian cohorts: the AusDiab Study and the Tromsø study.

https://arctichealth.org/en/permalink/ahliterature262595
Source
Nutr J. 2015 May 14;14(1):49
Publication Type
Article
Date
May-14-2015
Author
Svetlana N Zykova
Hilde M Storhaug
Ingrid Toft
Steven J Chadban
Trond G Jenssen
Sarah L White
Source
Nutr J. 2015 May 14;14(1):49
Date
May-14-2015
Language
English
Publication Type
Article
Abstract
Hyperuricemia can lead to gout, and may be a risk factor for cardiovascular events, hypertension, diabetes and renal disease. There is well-known link between gout and habitual intake of meat and seafood, however the association between hyperuricemia and micro-and macro-nutrient intake has not been established.
We studied associations between intakes of food categories, macro-and micronutrients and serum uric acid (SUA) levels in two cross-sectional surveys of Caucasian adults deriving from different food traditions: Australian Diabetes, Obesity and Lifestyle Study 1999/00 (n=9734, age 25-91) and Tromsø Study 4 1994/95 (n?=?3032, age 25-69). Dietary intake was calculated from self-administered Food Frequency Questionnaires. In some analyses we stratified according to abdominal obesity status and gender.
In both cohorts, lower levels of SUA were found in subjects with higher consumption of carbohydrates, calcium and vitamin B2, while higher fat intake was associated with higher SUA, after adjustment for age, body mass index, estimated glomerular filtration rate, physical activity, total energy intake, use of diuretics, presence of hypertension, diabetes and gout. Among individual food items, high consumption of dairy products, high-fibre bread, cereals and fruits were associated with lower SUA in most subject groups while consumption of meat, eggs, beer and spirits, but not wine, with elevated levels.
Healthy food choices with high intake of carbohydrates, dairy products, fiber and micronutrient-rich foods, and limited intake of fat, beer and spirits, might be recommended to prevent high SUA. Dietary factors seem to have qualitatively similar impact on SUA in obese and non-obese men and women from Australia and Norway.
PubMed ID
25971955 View in PubMed
Less detail

Elevated blood pressure is not associated with accelerated glomerular filtration rate decline in the general non-diabetic middle-aged population.

https://arctichealth.org/en/permalink/ahliterature272834
Source
Kidney Int. 2016 May 14;
Publication Type
Article
Date
May-14-2016
Author
Bjørn O Eriksen
Vidar T N Stefansson
Trond G Jenssen
Ulla D Mathisen
Jørgen Schei
Marit D Solbu
Tom Wilsgaard
Toralf Melsom
Source
Kidney Int. 2016 May 14;
Date
May-14-2016
Language
English
Publication Type
Article
Abstract
Although hypertension is a risk factor for end-stage renal disease, this complication develops in only a minority of hypertensive patients. Whether non-malignant hypertension itself is sufficient to cause reduced glomerular filtration rate (GFR) is unclear. Therefore, we investigated whether elevated blood pressure (BP) was associated with accelerated GFR decline in the general population. The study was based on the Renal Iohexol Clearance Survey in Tromsø 6 (RENIS-T6), which included a representative sample of 1594 individuals aged 50 to 62 years from the general population without baseline diabetes or kidney or cardiovascular disease. GFR was measured as iohexol clearance at baseline and follow-up after a median observation time of 5.6 years. BP was measured according to a standardized procedure. The mean (SD) GFR decline rate was 0.95 (2.23) ml/min/yr. In multivariable adjusted linear mixed regressions with either baseline systolic or diastolic BP as the independent variable, there were no statistically significant associations with GFR decline. Thus, elevated BP is not associated with accelerated mean GFR decline in the general middle-aged population. Hence, additional genetic and environmental factors are probably necessary for elevated BP to develop manifest chronic kidney disease in some individuals.
PubMed ID
27188503 View in PubMed
Less detail

Gender differences in the association of syndecan-4 with myocardial infarction: The population-based Tromsø Study.

https://arctichealth.org/en/permalink/ahliterature295234
Source
Atherosclerosis. 2018 Sep 15; 278:166-173
Publication Type
Journal Article
Date
Sep-15-2018
Author
Marit D Solbu
Svein O Kolset
Trond G Jenssen
Tom Wilsgaard
Maja-Lisa Løchen
Ellisiv B Mathiesen
Toralf Melsom
Bjørn O Eriksen
Trine M Reine
Author Affiliation
Section of Nephrology, University Hospital of North Norway, Tromsø, Norway; Metabolic and Renal Research Group, UiT The Arctic University of Norway, Tromsø, Norway. Electronic address: marit.solbu@unn.no.
Source
Atherosclerosis. 2018 Sep 15; 278:166-173
Date
Sep-15-2018
Language
English
Publication Type
Journal Article
Abstract
Cardiovascular disease is a common cause of morbidity and mortality, with gender differences in pathophysiology. The endothelial glycocalyx maintains vascular integrity, and glycocalyx shedding reflects endothelial dysfunction and early atherosclerosis. Syndecan-1 and -4 are components of the glycocalyx, and increased serum levels indicate glycocalyx damage. We hypothesised that increased serum syndecan-1 and -4 were independently associated with myocardial infarction (MI), ischaemic stroke and all-cause mortality in men and women from a general population.
Using a case-cohort design, we included 1495 participants from the Tromsø Study 2001-02. Syndecan-1 and -4 were measured in serum. Baseline variables also included age, gender, cardiovascular risk factors and urinary albumin-creatinine ratio (ACR). Hazard ratios were assessed using multivariable Cox regression models.
Between baseline in 2001-02 and December 2007 fatal or non-fatal MI was experienced by 328 and ischaemic stroke by 191 subjects, and 423 participants died. Syndecan-4 was independently associated with MI (hazard ratio per 10?ng/mL increase 1.32; 95% confidence interval 1.06-1.63), but not ischaemic stroke and mortality, and the associations were unchanged by adjustment for urinary ACR. Interaction between syndecan-4 and sex was borderline significant, and in gender-specific analysis, syndecan-4 was associated with MI in women only. Syndecan-1 was not associated with any endpoint.
Syndecan-4 was associated with incident MI, and the association was stronger in women than in men. This suggests a link between endothelial glycocalyx shedding and coronary heart disease in women. Use of syndecan-4 as a risk marker in clinical setting needs further investigation.
PubMed ID
30278359 View in PubMed
Less detail

GFR in Healthy Aging: an Individual Participant Data Meta-Analysis of Iohexol Clearance in European Population-Based Cohorts.

https://arctichealth.org/en/permalink/ahliterature305702
Source
J Am Soc Nephrol. 2020 07; 31(7):1602-1615
Publication Type
Journal Article
Meta-Analysis
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Date
07-2020
Author
Bjørn O Eriksen
Runolfur Palsson
Natalie Ebert
Toralf Melsom
Markus van der Giet
Vilmundur Gudnason
Olafur S Indridasson
Lesley A Inker
Trond G Jenssen
Andrew S Levey
Marit D Solbu
Hocine Tighiouart
Elke Schaeffner
Author Affiliation
Metabolic and Renal Research Group, University of Tromsø - The Arctic University of Norway, Tromsø, Norway bjorn.odvar.eriksen@unn.no.
Source
J Am Soc Nephrol. 2020 07; 31(7):1602-1615
Date
07-2020
Language
English
Publication Type
Journal Article
Meta-Analysis
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Keywords
Age Factors
Aged
Aged, 80 and over
Aging - physiology
Contrast Media - pharmacokinetics
Female
Germany
Glomerular Filtration Rate
Health status
Humans
Iceland
Iohexol - pharmacokinetics
Male
Metabolic Clearance Rate
Middle Aged
Norway
Sex Factors
Abstract
Population mean GFR is lower in older age, but it is unknown whether healthy aging is associated with preserved rather than lower GFR in some individuals.
We investigated the cross-sectional association between measured GFR, age, and health in persons aged 50-97 years in the general population through a meta-analysis of iohexol clearance measurements in three large European population-based cohorts. We defined a healthy person as having no major chronic disease or risk factors for CKD and all others as unhealthy. We used a generalized additive model to study GFR distribution by age according to health status.
There were 935 (22%) GFR measurements in persons who were healthy and 3274 (78%) in persons who were unhealthy. The mean GFR was lower in older age by -0.72 ml/min per 1.73 m2 per year (95% confidence interval [95% CI], -0.96 to -0.48) for men who were healthy versus -1.03 ml/min per 1.73 m2 per year (95% CI, -1.25 to -0.80) for men who were unhealthy, and by -0.92 ml/min per 1.73 m2 per year (95% CI, -1.14 to -0.70) for women who were healthy versus -1.22 ml/min per 1.73 m2 per year (95% CI, -1.43 to -1.02) for women who were unhealthy. For healthy and unhealthy people of both sexes, both the 97.5th and 2.5th GFR percentiles exhibited a negative linear association with age.
Healthy aging is associated with a higher mean GFR compared with unhealthy aging. However, both the mean and 97.5 percentiles of the GFR distribution are lower in older persons who are healthy than in middle-aged persons who are healthy. This suggests that healthy aging is not associated with preserved GFR in old age.
PubMed ID
32499396 View in PubMed
Less detail

21 records – page 1 of 3.