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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
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Cites: J Am Soc Nephrol. 2006 Mar;17(3):846-53 PMID 16452492
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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
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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

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

Metabolic syndrome but not obesity measures are risk factors for accelerated age-related glomerular filtration rate decline in the general population.

https://arctichealth.org/en/permalink/ahliterature296905
Source
Kidney Int. 2018 05; 93(5):1183-1190
Publication Type
Journal Article
Observational Study
Date
05-2018
Author
Vidar T N Stefansson
Jørgen Schei
Marit D Solbu
Trond G Jenssen
Toralf Melsom
Bjørn O Eriksen
Author Affiliation
Metabolic and Renal Research Group, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway. Electronic address: vidar.stefansson@uit.no.
Source
Kidney Int. 2018 05; 93(5):1183-1190
Date
05-2018
Language
English
Publication Type
Journal Article
Observational Study
Keywords
Age Factors
Biomarkers - blood
Blood Glucose - analysis
Blood pressure
Body mass index
Cholesterol, HDL - blood
Disease Progression
Female
Glomerular Filtration Rate
Humans
Kidney - physiopathology
Kidney Diseases - diagnosis - etiology - physiopathology
Longitudinal Studies
Male
Metabolic Syndrome - blood - complications - diagnosis - physiopathology
Middle Aged
Norway
Obesity - blood - complications - diagnosis - physiopathology
Risk assessment
Risk factors
Time Factors
Triglycerides - blood
Waist Circumference
Waist-Hip Ratio
Abstract
Rapid age-related glomerular filtration rate (GFR) decline increases the risk of end-stage renal disease, and a low GFR increases the risk of mortality and cardiovascular disease. High body mass index and the metabolic syndrome are well-known risk factors for patients with advanced chronic kidney disease, but their role in accelerating age-related GFR decline independent of cardiovascular disease, hypertension and diabetes is not adequately understood. We studied body mass index, waist circumference, waist-hip ratio and metabolic syndrome as risk factors for accelerated GFR decline in 1261 middle-aged people representative of the general population without diabetes, cardiovascular disease or kidney disease. GFR was measured as iohexol clearance at baseline and repeated after a median of 5.6 years. Metabolic syndrome was defined as fulfilling three out of five criteria, based on waist circumference, blood pressure, glucose, high-density lipoprotein cholesterol and triglycerides. The mean GFR decline rate was 0.95 ml/min/year. Neither the body mass index, waist circumference nor waist-hip ratio predicted statistically significant changes in age-related GFR decline, but individuals with baseline metabolic syndrome had a significant mean of 0.30 ml/min/year faster decline than individuals without metabolic syndrome in a multivariable adjusted linear regression model. This association was mainly driven by the triglyceride criterion of metabolic syndrome, which was associated with a significant 0.36 ml/min/year faster decline when analyzed separately. Results differed significantly when GFR was estimated using creatinine and/or cystatin C. Thus, metabolic syndrome, but not the body mass index, waist circumference or waist-hip ratio, is an independent risk factor for accelerated age-related GFR decline in the general population.
PubMed ID
29395334 View in PubMed
Less detail

Office and Ambulatory Heart Rate as Predictors of Age-Related Kidney Function Decline.

https://arctichealth.org/en/permalink/ahliterature295555
Source
Hypertension. 2018 Sep; 72(3):594-601
Publication Type
Journal Article
Date
Sep-2018
Author
Bjørn O Eriksen
Silje Småbrekke
Trond G Jenssen
Ulla D Mathisen
Jon V Norvik
Jørgen Schei
Henrik Schirmer
Marit D Solbu
Vidar T N Stefansson
Toralf Melsom
Author Affiliation
From the Metabolic and Renal Research Group, UiT The Arctic University of Norway, Tromsø (B.O.E., S.S., T.G.J., U.D.M., J.V.N., J.S., M.D.S., V.T.N.S., T.M.).
Source
Hypertension. 2018 Sep; 72(3):594-601
Date
Sep-2018
Language
English
Publication Type
Journal Article
Abstract
The decline in glomerular filtration rate (GFR) associated with aging is one of the most important predisposing causes of kidney failure in old age. Identifying persons at risk for accelerated GFR decline is an essential first step in the development of preventive measures to preserve kidney function in the elderly. Heart rate (HR) has not yet been studied as a risk factor for GFR decline in the general population. In the RENIS-T6 (Renal Iohexol-Clearance Survey in Tromsø 6), we measured baseline ambulatory HR and GFR as iohexol clearance in a representative, middle-aged cohort of 1627 persons without self-reported diabetes mellitus, cardiovascular disease, or kidney disease. In the RENIS-FU (RENIS Follow-Up Study), we repeated the GFR measurements and calculated the rate of GFR decline in 81% of the participants after a median follow-up of 5.6 years. The unadjusted mean rate of GFR decline was 0.96 mL/min per year. In multivariable-adjusted linear mixed models, 10 bpm higher ambulatory 24-hour and daytime HRs and office HR were associated with steeper GFR decline rates of 0.20 to 0.21 mL/min per year ( P=0.01). The odds ratio for predicting a rate of GFR decline twice that of the population mean in a fully adjusted model was 1.24 ( P=0.01) for ambulatory 24-hour HR. Office HR was also an independent predictor of a steeper rate of GFR decline. HR may be a useful biomarker to identify persons at risk of accelerated GFR decline.
PubMed ID
30354758 View in PubMed
Less detail

Office and Ambulatory Heart Rate as Predictors of Age-Related Kidney Function Decline.

https://arctichealth.org/en/permalink/ahliterature299317
Source
Hypertension. 2018 09; 72(3):594-601
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
09-2018
Author
Bjørn O Eriksen
Silje Småbrekke
Trond G Jenssen
Ulla D Mathisen
Jon V Norvik
Jørgen Schei
Henrik Schirmer
Marit D Solbu
Vidar T N Stefansson
Toralf Melsom
Author Affiliation
From the Metabolic and Renal Research Group, UiT The Arctic University of Norway, Tromsø (B.O.E., S.S., T.G.J., U.D.M., J.V.N., J.S., M.D.S., V.T.N.S., T.M.).
Source
Hypertension. 2018 09; 72(3):594-601
Date
09-2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Aging
Blood Pressure - physiology
Cohort Studies
Female
Follow-Up Studies
Glomerular Filtration Rate - physiology
Health Surveys - methods - statistics & numerical data
Heart Rate - physiology
Humans
Kidney - physiopathology
Kidney Failure, Chronic - diagnosis - physiopathology
Male
Middle Aged
Prognosis
Risk factors
Abstract
The decline in glomerular filtration rate (GFR) associated with aging is one of the most important predisposing causes of kidney failure in old age. Identifying persons at risk for accelerated GFR decline is an essential first step in the development of preventive measures to preserve kidney function in the elderly. Heart rate (HR) has not yet been studied as a risk factor for GFR decline in the general population. In the RENIS-T6 (Renal Iohexol-Clearance Survey in Tromsø 6), we measured baseline ambulatory HR and GFR as iohexol clearance in a representative, middle-aged cohort of 1627 persons without self-reported diabetes mellitus, cardiovascular disease, or kidney disease. In the RENIS-FU (RENIS Follow-Up Study), we repeated the GFR measurements and calculated the rate of GFR decline in 81% of the participants after a median follow-up of 5.6 years. The unadjusted mean rate of GFR decline was 0.96 mL/min per year. In multivariable-adjusted linear mixed models, 10 bpm higher ambulatory 24-hour and daytime HRs and office HR were associated with steeper GFR decline rates of 0.20 to 0.21 mL/min per year ( P=0.01). The odds ratio for predicting a rate of GFR decline twice that of the population mean in a fully adjusted model was 1.24 ( P=0.01) for ambulatory 24-hour HR. Office HR was also an independent predictor of a steeper rate of GFR decline. HR may be a useful biomarker to identify persons at risk of accelerated GFR decline.
PubMed ID
30354758 View in PubMed
Less detail

Residual Associations of Inflammatory Markers with eGFR after Accounting for Measured GFR in a Community-Based Cohort without CKD.

https://arctichealth.org/en/permalink/ahliterature268114
Source
Clin J Am Soc Nephrol. 2015 Dec 14;
Publication Type
Article
Date
Dec-14-2015
Author
Jørgen Schei
Vidar T N Stefansson
Ulla Dorte Mathisen
Bjørn O Eriksen
Marit D Solbu
Trond G Jenssen
Toralf Melsom
Source
Clin J Am Soc Nephrol. 2015 Dec 14;
Date
Dec-14-2015
Language
English
Publication Type
Article
Abstract
eGFR on the basis of creatinine (eGFRcre) associates differently with cardiovascular disease and mortality than eGFR on the basis of cystatin C (eGFRcys). This may be related to risk factors affecting the level of creatinine and cystatin C along non-GFR pathways, which may confound the association between eGFR and outcome. Nontraditional risk factors are usually not measured in epidemiologic studies of eGFR and cannot be adjusted for to reduce confounding. We examined whether the inflammatory markers soluble TNF receptor type 2 (sTNFR2), C-reactive protein (CRP), and fibrinogen associated differently with eGFR than with measured GFR (mGFR).
GFR was measured by iohexol clearance in 1627 middle-aged participants without kidney disease, diabetes, or cardiovascular disease enrolled in the Renal Iohexol Clearance Survey Study from the Sixth Tromsø Study between 2007 and 2009. Generalized estimating equations were used to assess the residual associations between eGFR (eGFRcre, eGFRcys, and eGFR on the basis of creatinine and cystatin C) and the inflammatory markers relative to mGFR.
sTNFR2, CRP, and fibrinogen were associated with a higher eGFRcre after accounting for mGFR in multivariable-adjusted models (2.63 ml/min per 1.73 m(2); 95% confidence interval [95% CI], 2.1 to 3.2 per SD increase in sTNFR2, 0.93 ml/min per 1.73 m(2); 95% CI, 0.3 to 1.5 per SD increase in log CRP, and 1.19 ml/min per 1.73 m(2); 95% CI, 0.6 to 1.8 per SD increase in fibrinogen). sTNFR2 and CRP were inversely associated with eGFRcys (-1.4 ml/min per 1.73 m(2); 95% CI, -2.1 to -0.6 per SD increase in sTNFR2, and -0.76 ml/min per 1.73 m(2); 95% CI, -1.4 to -0.1 per SD increase in log CRP).
eGFRcre and eGFRcys are associated with inflammatory factors after accounting for mGFR but in opposite directions. These non-GFR-related associations may bias risk estimates by eGFR and, in part, explain the different risks predicted by eGFRcre and eGFRcys in longitudinal studies.
PubMed ID
26668020 View in PubMed
Less detail

7 records – page 1 of 1.