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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
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Association of Increasing GFR with Change in Albuminuria in the General Population.

https://arctichealth.org/en/permalink/ahliterature276462
Source
Clin J Am Soc Nephrol. 2016 Sep 28;
Publication Type
Article
Date
Sep-28-2016
Author
Toralf Melsom
Vidar Stefansson
Jørgen Schei
Marit Solbu
Trond Jenssen
Tom Wilsgaard
Bjørn O Eriksen
Source
Clin J Am Soc Nephrol. 2016 Sep 28;
Date
Sep-28-2016
Language
English
Publication Type
Article
Abstract
Hyperfiltration at the single-nephron level has been proposed as an early stage of kidney dysfunction of different origins. Evidence supporting this hypothesis in humans is lacking, because there is no method of measuring single-nephron GFR in humans. However, increased whole-kidney GFR in the same individual implies an increased single-nephron GFR, because the number of nephrons does not increase with age. We hypothesized that an increase in GFR would be associated with an increased albumin-to-creatinine ratio in a cohort of the general population.
We measured GFR by iohexol clearance at baseline in 2007-2009 and follow-up after 5.6 years in a representative sample of 1246 persons (aged 50-62 years) who were nondiabetic from the general population of Tromso, northern Norway. Participants were without cardiovascular disease, kidney disease, or diabetes at baseline. We investigated the association between change in GFR and change in albumin-to-creatinine ratio. Increased GFR was defined as a positive change in GFR (change in GFR>0 ml/min) from baseline to follow-up. An albumin-to-creatinine ratio >30 mg/g was classified as albuminuria.
Change in GFR was positively associated with a change in albumin-to-creatinine ratio in the entire cohort in the multiple linear regression. The albumin-to-creatinine ratiofollow-up-to-albumin-to-creatinine ratiobaseline ratio increased by 8.0% (95% confidence interval, 1.4 to 15.0) per SD increase in change in GFR. When participants with increased GFR (n=343) were compared with those with a reduced GFR (n=903), the ratio increased by 16.3% (95% confidence interval, 1.1 to 33.7). The multivariable adjusted odds ratio for incident albuminuria (n=14) was 4.98 (95% confidence interval, 1.49 to 16.13) for those with an increased GFR (yes/no).
Increasing GFR is associated with an increase in albumin-to-creatinine ratio and incident albuminuria in the general nondiabetic population. These findings support single-nephron hyperfiltration as a risk factor for albuminuria in the general population.
PubMed ID
27683625 View in PubMed
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Association of TNF Receptor 2 and CRP with GFR Decline in the General Nondiabetic Population.

https://arctichealth.org/en/permalink/ahliterature279921
Source
Clin J Am Soc Nephrol. 2017 Feb 02;
Publication Type
Article
Date
Feb-02-2017
Author
Jørgen Schei
Vidar Tor Nyborg Stefansson
Bjørn Odvar Eriksen
Trond Geir Jenssen
Marit Dahl Solbu
Tom Wilsgaard
Toralf Melsom
Source
Clin J Am Soc Nephrol. 2017 Feb 02;
Date
Feb-02-2017
Language
English
Publication Type
Article
Abstract
Higher levels of inflammatory markers have been associated with renal outcomes in diabetic populations. We investigated whether soluble TNF receptor 2 (TNFR2) and high-sensitivity C-reactive protein (hsCRP) were associated with the age-related GFR decline in a nondiabetic population using measured GFR (mGFR).
A representative sample of 1590 middle-aged people from the general population without prevalent kidney disease, diabetes, or cardiovascular disease were enrolled in the Renal Iohexol-Clearance Survey in Tromsø 6 (RENIS-T6) between 2007 and 2009. After a median of 5.6 years, 1296 persons were included in the Renal Iohexol-Clearance Survey Follow-Up Study. GFR was measured using iohexol clearance at baseline and follow-up.
The mean decline of mGFR during the period was -0.84 ml/min per 1.73 m(2) per year. There were 133 participants with rapid mGFR decline, defined as an annual mGFR loss >3.0 ml/min per 1.73 m(2), and 26 participants with incident CKD, defined as mGFR
PubMed ID
28153935 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: Am J Kidney Dis. 2012 Jan;59(1):41-9 PMID 22000727
Cites: J Hypertens. 1995 Mar;13(3):357-65 PMID 7622857
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Cites: Hypertension. 2000 Mar;35(3):822-6 PMID 10720601
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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
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Cites: JAMA. 2002 Nov 20;288(19):2421-31 PMID 12435255
Cites: Nephron. 2015;131(3):175-84 PMID 26426198
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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

Central obesity associates with renal hyperfiltration in the non-diabetic general population: a cross-sectional study.

https://arctichealth.org/en/permalink/ahliterature277790
Source
BMC Nephrol. 2016 Nov 10;17(1):172
Publication Type
Article
Date
Nov-10-2016
Author
Vidar Tor Nyborg Stefansson
Jørgen Schei
Trond Geir Jenssen
Toralf Melsom
Bjørn Odvar Eriksen
Source
BMC Nephrol. 2016 Nov 10;17(1):172
Date
Nov-10-2016
Language
English
Publication Type
Article
Abstract
Obesity is a risk factor for end-stage renal disease. Renal hyperfiltration, defined as an abnormally high glomerular filtration rate (GFR), is a link in the causal chain between diabetes and chronic kidney disease. Whether obesity is associated with hyperfiltration in the non-diabetic general population, remains unresolved due to a lack of consensus regarding the definition of hyperfiltration and the limited precision of high-range GFR estimations with creatinine and/or cystatin C.
1555 middle-aged participants without diabetes, renal or cardiovascular disease were enrolled from the general population in the Renal Iohexol Clearance Survey from the 6th Tromsø Study (RENIS-T6) between 2007 and 2009. Obesity was assessed using the body mass index (BMI), waist circumference (WC) and the waist-hip ratio (WHR). GFR was measured by iohexol clearance. Dichotomous variables for hyperfiltration were based on two alternative definitions using unadjusted GFR (mL/min) above the 90th percentile. The 90th percentile was age-, sex- and height-specific in one definition and age-, sex-, height- and weight-specific in the other.
In multivariable adjusted logistic regression models, only WHR was consistently associated with hyperfiltration based on both definitions. For the definition based on the age-, sex-, height- and weight-specific 90th percentile, the association with the WHR (odds ratios (95 % confidence intervals)) for hyperfiltration was 1.48 (1.08-2.02) per 0.10 WHR increase.
Central obesity is associated with hyperfiltration in the general population. The WHR may serve as a better indicator of the renal effects of obesity than BMI or WC.
PubMed ID
27832768 View in PubMed
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Comparability of Plasma Iohexol Clearance Across Population-Based Cohorts.

https://arctichealth.org/en/permalink/ahliterature307515
Source
Am J Kidney Dis. 2020 07; 76(1):54-62
Publication Type
Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Date
07-2020
Author
Bjørn O Eriksen
Elke Schaeffner
Toralf Melsom
Natalie Ebert
Markus van der Giet
Vilmundur Gudnason
Olafur S Indridasson
Amy B Karger
Andrew S Levey
Mirjam Schuchardt
Liv K Sørensen
Runolfur Palsson
Author Affiliation
Metabolic and Renal Research Group, UiT The Arctic University of Norway, Tromsø, Norway. Electronic address: bjorn.odvar.eriksen@unn.no.
Source
Am J Kidney Dis. 2020 07; 76(1):54-62
Date
07-2020
Language
English
Publication Type
Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Keywords
Aged
Aged, 80 and over
Aging - blood
Biomarkers - blood
Cohort Studies
Contrast Media - metabolism
Cross-Sectional Studies
Female
Follow-Up Studies
Gene-Environment Interaction
Germany - epidemiology
Glomerular Filtration Rate - physiology
Humans
Iceland - epidemiology
Iohexol - metabolism
Kidney Function Tests - methods
Male
Metabolic Clearance Rate - physiology
Middle Aged
Norway - epidemiology
Population Surveillance
Abstract
Glomerular filtration rate (GFR) estimation based on creatinine or cystatin C level is currently the standard method for assessing GFR in epidemiologic research and clinical trials despite several important and well-known limitations. Plasma iohexol clearance has been proposed as an inexpensive method for measuring GFR that could replace estimated GFR in many research projects. However, lack of standardization for iohexol assays and the use of different protocols such as single- and multiple-sample methods could potentially hamper comparisons across studies. We compared iohexol assays and GFR measurement protocols in 3 population-based European cohorts.
Cross-sectional investigation.
Participants in the Age, Gene/Environment Susceptibility-Kidney Study (AGES-Kidney; n=805), the Berlin Initiative Study (BIS, n=570), and the Renal Iohexol Clearance Survey Follow-up Study (RENIS-FU; n=1,324).
High-performance liquid chromatography analyses of iohexol. Plasma iohexol clearance calculated using single- versus multiple-sample protocols.
Measures of agreement between methods.
Frozen samples from the 3 studies were obtained and iohexol concentrations were remeasured in the laboratory at the University Hospital of North Norway. Lin's concordance correlation coefficient ? was>0.96 and Cb (accuracy) was>0.99 for remeasured versus original serum iohexol concentrations in all 3 cohorts, and Passing-Bablok regression did not find differences between measurements, except for a slope of 1.025 (95% CI, 1.006-1.046) for the log-transformed AGES-Kidney measurements. The multiple-sample iohexol clearance measurements in AGES-Kidney and BIS were compared with single-sample GFRs derived from the same iohexol measurements. Mean bias for multiple-sample relative to single-sample GFRs in AGES-Kidney and BIS were-0.25 and-0.15mL/min, and 99% and 97% of absolute differences were within 10% of the multiple-sample result, respectively.
Lack of comparison with an independent gold-standard method.
Agreement between the iohexol assays and clearance protocols in the 3 investigated cohorts was substantial. Our findings indicate that plasma iohexol clearance measurements can be compared across these studies.
PubMed ID
31879216 View in PubMed
Less detail

Cystatin C as risk factor for cardiovascular events and all-cause mortality in the general population. The Tromsø Study.

https://arctichealth.org/en/permalink/ahliterature128439
Source
Nephrol Dial Transplant. 2012 Jul;27(7):2780-7
Publication Type
Article
Date
Jul-2012
Author
Ingrid Toft
Marit Solbu
Jens Kronborg
Ulla D Mathisen
Bjørn O Eriksen
Hilde Storhaug
Toralf Melsom
Maja-Lisa Løchen
Ellisiv B Mathiesen
Inger Njølstad
Tom Wilsgaard
Jan Brox
Author Affiliation
Department of Nephrology, University Hospital of North Norway, and Department of Clinical Medicine, University of Tromsø, Tromsø, Norway. Ingrid.Toft@unn.no
Source
Nephrol Dial Transplant. 2012 Jul;27(7):2780-7
Date
Jul-2012
Language
English
Publication Type
Article
Keywords
Aged
Cardiovascular Diseases - epidemiology - etiology - metabolism - mortality
Cystatin C - metabolism
Female
Follow-Up Studies
Glomerular Filtration Rate
Humans
Male
Middle Aged
Norway - epidemiology
Prognosis
Prospective Studies
Risk factors
Survival Rate
Abstract
Glomerular filtration rate60 mL/min/1.73 m2) and possibly a more sensitive marker for cardiovascular risk and all-cause mortality. We examined the association of cystatin C with cardiovascular morbidity and all-cause mortality in a prospective population-based study.
Cystatin C was measured in 2852 men and 3153 women in the Tromsø Study 1994/95. Gender-specific associations during 12 years of follow-up for all-cause mortality and 9.5 years for myocardial infarction (MI) and ischaemic stroke were assessed (Cox proportional hazard ratios, HRs).
During follow-up, 591 MIs, 293 ischaemic strokes and 1262 deaths occurred. In women, HR for all-cause mortality was increased in the upper cystatin C quartile (=0.93 mg/L) compared with the lowest quartile (=0.73 mg/L); 1.38, 95% confidence interval 1.04-1.84. A significant interaction with gender was observed. One SD (0.17 mg/L) increase in cystatin C was associated with 9% higher risk of death in women, also when persons with a cancer history were excluded. Crude HRs for MI and ischaemic stroke were increased in both genders, but the associations did not persist after multivariable adjustments. No independent associations with end points were observed in non-gender-specific analyses.
Cystatin C was not independently associated with fatal and non-fatal MI or ischaemic stroke in the general population. However, cystatin C was a risk factor for all-cause mortality in women.
PubMed ID
22207328 View in PubMed
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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
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27 records – page 1 of 3.