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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
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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
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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

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
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Estimated and Measured GFR Associate Differently with Retinal Vasculopathy in the General Population.

https://arctichealth.org/en/permalink/ahliterature266562
Source
Nephron. 2015 Oct 2;
Publication Type
Article
Date
Oct-2-2015
Author
Bjørn Odvar Eriksen
Maja-Lisa Løchen
Kjell Arne Arntzen
Geir Bertelsen
Britt-Ann Winther Eilertsen
Therese von Hanno
Marit Herder
Trond Geir Jenssen
Ulla Dorte Mathisen
Toralf Melsom
Inger Njølstad
Marit D Solbu
Ellisiv B Mathiesen
Source
Nephron. 2015 Oct 2;
Date
Oct-2-2015
Language
English
Publication Type
Article
Abstract
Estimated glomerular filtration rate (eGFR) is used extensively in epidemiological research. Validations of eGFR have demonstrated acceptable performance, but the dependence of creatinine and cystatin C on non-GFR factors could confound associations with disease. Few studies have investigated this issue in direct comparison with measured GFR (mGFR). We compared the associations between eGFR and mGFR and retinal vasculopathy, a marker of systemic microvasculopathy.
Iohexol clearance and retinal photography were examined in the Renal Iohexol Clearance Survey in Tromsø 6, which consists of a representative sample of middle-aged persons from the general population. A total of 1,553 persons without self-reported kidney disease, cardiovascular disease or diabetes were investigated. Three eGFR equations based on creatinine and/or cystatin C from the Chronic Kidney Disease Epidemiology Collaboration were studied. Differences between eGFR and mGFR were analyzed with seemingly unrelated regression methods.
mGFR in the lowest quartile was associated with an increased multivariable-adjusted odds ratio of retinopathy (OR 1.86, 95% CI 1.16-2.97), but not with retinal artery or vein diameters. eGFR based on cystatin C (eGFRcys) was consistently biased relative to mGFR in its associations with retinal vessel diameters across different models. eGFR based on creatinine (eGFRcrea) and eGFR based on both creatinine and cystatin C were also biased in several of these models (p
PubMed ID
26426198 View in PubMed
Less detail

Estimated Glomerular Filtration Rate (eGFR) based on cystatin C was associated with increased risk of hip and proximal humerus fractures in women and decreased risk of hip fracture in men, whereas eGFR based on creatinine was not associated with fracture risk in both sexes: The Tromsø Study.

https://arctichealth.org/en/permalink/ahliterature311679
Source
Bone. 2021 Jul; 148:115960
Publication Type
Journal Article
Date
Jul-2021
Author
Sofie K Nordvåg
Marit D Solbu
Toralf Melsom
Frida I Nissen
Camilla Andreasen
Tove T Borgen
Bjørn O Eriksen
Ragnar M Joakimsen
Åshild Bjørnerem
Author Affiliation
Women's Health and Perinatalogy Research Group, Department of Clinical Medicine, UiT The Arctic University of Norway, Tromsø, Norway.
Source
Bone. 2021 Jul; 148:115960
Date
Jul-2021
Language
English
Publication Type
Journal Article
Abstract
Patients with end-stage kidney disease have an increased fracture risk. Whether mild to moderate reductions in kidney function is associated with increased fracture risk is uncertain. Results from previous studies may be confounded by muscle mass because of the use of creatinine-based estimates of the glomerular filtration rate (eGFRcre). We tested the hypothesis that lower eGFR within the normal range of kidney function based on serum cystatin C (eGFRcys) or both cystatin C and creatinine (eGFRcrecys) predict fractures better than eGFR based on creatinine (eGFRcre).
In the Tromsø Study 1994-95, a cohort of 3016 women and 2836 men aged 50-84 years had eGFRcre, eGFRcys and eGFRcrecys estimated using the Chronic Kidney Disease Epidemiology Collaboration equations. Hazard ratios (HRs) (95% confidence intervals) for fracture were calculated in Cox's proportional hazards models and adjusted for age, height, body mass index, bone mineral density, diastolic blood pressure, smoking, physical activity, previous fracture, diabetes and cardiovascular disease.
During a median of 14.6 years follow-up, 232, 135 and 394 women and 118, 35 and 65 men suffered incident hip, proximal humerus and wrist fractures. In women, lower eGFRcre did not predict fracture, but the risk for hip and proximal humerus fracture increased per standard deviation (SD) lower eGFRcys (HRs 1.36 (1.16-1.60) and 1.33 (1.08-1.63)) and per SD lower eGFRcrecys (HRs 1.25 (1.08-1.45) and 1.30 (1.07-1.57)). In men, none of the eGFR estimates were related to increased fracture risk. In contrast, eGFRcys and eGFRcrecys were inversely associated with hip fracture risk (HRs 0.85 (0.73-0.99) and 0.82 (0.68-0.98)).
In women, each SD lower eGFRcys and eGFRcrecys increased the risk of hip and proximal humerus fracture by 25-36%, whereas eGFRcre did not. In men, none of the estimates of eGFR were related to increased fracture risk, and each SD lower eGFRcys and eGFRcrecys decreased the risk of hip fracture by 15-18%. The findings particularly apply to a cohort of generally healthy individuals with a normal kidney function. In future studies, the association of measured GFR using the gold standard method of iohexol clearance with fractures risk should be examined for causal inference. More clinical research is needed before robust clinical inferences can be made.
PubMed ID
33864977 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
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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
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Impaired fasting glucose is associated with renal hyperfiltration in the general population.

https://arctichealth.org/en/permalink/ahliterature134380
Source
Diabetes Care. 2011 Jul;34(7):1546-51
Publication Type
Article
Date
Jul-2011
Author
Toralf Melsom
Ulla Dorte Mathisen
Ole C Ingebretsen
Trond G Jenssen
Inger Njølstad
Marit D Solbu
Ingrid Toft
Bjørn O Eriksen
Author Affiliation
Department of Medical Biochemistry, University Hospital of North Norway, and the Department of Clinical Medicine, University of Tromsø, Tromsø, Norway. toralf.melsom@unn.no
Source
Diabetes Care. 2011 Jul;34(7):1546-51
Date
Jul-2011
Language
English
Publication Type
Article
Keywords
Blood Glucose - metabolism
Fasting
Female
Glomerular Filtration Rate
Glucose Intolerance - complications - physiopathology
Hemoglobin A, Glycosylated - metabolism
Humans
Hyperglycemia - complications - physiopathology
Hyperinsulinism - physiopathology
Iohexol - diagnostic use
Male
Middle Aged
Renal Insufficiency, Chronic - etiology
Abstract
Increased glomerular filtration rate (GFR), also called hyperfiltration, is a proposed mechanism for renal injury in diabetes. The causes of hyperfiltration in individuals without diabetes are largely unknown, including the possible role of borderline hyperglycemia. We assessed whether impaired fasting glucose (IFG; 5.6-6.9 mmol/L), elevated HbA1c, or hyperinsulinemia are associated with hyperfiltration in the general middle-aged population.
A total of 1,560 individuals, aged 50-62 years without diabetes, were included in the Renal Iohexol Clearance Survey in Tromsø 6 (RENIS-T6). GFR was measured as single-sample plasma iohexol clearance. Hyperfiltration was defined as GFR>90th percentile, adjusted for sex, age, weight, height, and use of renin-angiotensin system inhibitors.
Participants with IFG had a multivariable-adjusted odds ratio of 1.56 (95% CI 1.07-2.25) for hyperfiltration compared with individuals with normal fasting glucose. Odds ratios (95% CI) of hyperfiltration calculated for a 1-unit increase in fasting plasma glucose (FPG) and HbA1c, after multivariable-adjustment, were 1.97 (1.36-2.85) and 2.23 (1.30-3.86). There was no association between fasting insulin levels and hyperfiltration. A nonlinear association between FPG and GFR was observed (df=3, P
Notes
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PubMed ID
21593291 View in PubMed
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