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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
Less detail

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: Kidney Int. 2013 Jun;83(6):1169-76 PMID 23423253
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Cites: Nephron. 2015;131(3):175-84 PMID 26426198
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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
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
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Prediabetes and Risk of Glomerular Hyperfiltration and Albuminuria in the General Nondiabetic Population: A Prospective Cohort Study.

https://arctichealth.org/en/permalink/ahliterature269189
Source
Am J Kidney Dis. 2015 Dec 16;
Publication Type
Article
Date
Dec-16-2015
Author
Toralf Melsom
Jørgen Schei
Vidar Tor Nyborg Stefansson
Marit Dahl Solbu
Trond Geir Jenssen
Ulla Dorte Mathisen
Tom Wilsgaard
Bjørn Odvar Eriksen
Source
Am J Kidney Dis. 2015 Dec 16;
Date
Dec-16-2015
Language
English
Publication Type
Article
Abstract
The role of prediabetes as a risk factor for hyperfiltration and albuminuria in persons who do not develop diabetes is unclear. The lack of evidence is mainly due to the difficulty of accurately assessing the glomerular filtration rate (GFR) in the near-normal range of GFR. We investigated whether prediabetes is an independent risk factor for glomerular hyperfiltration and high-normal urinary albumin-creatinine ratio (ACR) using measured GFR (mGFR) rather than estimated GFR.
Prospective cohort study based on the Renal Iohexol Clearance Survey in Tromsø 6 (RENIS-T6) and the RENIS Follow-Up Study. Median observation time was 5.6 years.
A representative sample of 1,261 persons without diabetes mellitus (DM) from the general population aged 50 to 62 years.
Prediabetes defined by fasting glucose and hemoglobin A1c according to levels suggested by the American Diabetes Association (preDMADA) and the International Expert Committee of 2009 (preDMIEC).
Change in mGFR; hyperfiltration defined as mGFR>90th percentile adjusted for age, sex, weight, and height; and high-normal ACR (>10mg/g) at follow-up.
GFR was measured with iohexol clearance.
Baseline fasting glucose, hemoglobin A1c, and both definitions of prediabetes were predictors of higher mGFR at follow-up and lower annual mGFR decline in multivariable-adjusted regression analyses. Participants with preDMIEC had an OR for hyperfiltration of 1.95 (95% CI, 1.20-3.17) and for high-normal ACR of 1.83 (95% CI, 1.04-3.22) at follow-up. We adjusted for cardiovascular risk factors including ambulatory blood pressure at baseline and change in use of antihypertensive medication between baseline and follow-up.
Only middle-aged white patients participated. There is no consensus on how to define glomerular hyperfiltration.
Our findings imply an independent role of prediabetes in the development of glomerular hyperfiltration and albuminuria. Prediabetes might be a target for early treatment to prevent chronic kidney disease in chronic hyperglycemia.
PubMed ID
26744126 View in PubMed
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