03275nas a2200589 4500008004100000022001400041245004900055210004800104260001300152300001100165490000700176520170100183653001601884653000901900653002201909653001501931653002101946653002501967653001501992653002802007653001502035653001402050653002402064653001102088653002502099653001102124653001402135653003102149653003102180653000902211653001502220653003002235653001402265653002002279653003202299653003002331653001602361653002202377100002402399700002002423700001602443700001802459700002002477700002102497700003202518700001702550700001702567700002202584700002002606700002402626856003502650 2005 eng d a1046-667300aCystatin C and subclinical brain infarction.0 aCystatin C and subclinical brain infarction c2005 Dec a3721-70 v163 a
Subclinical brain infarcts (SBI) are common in the elderly and are associated with covert neurologic and cognitive impairment. Although renal impairment is associated with accelerated cerebrovascular disease and an increased risk for clinically apparent brain infarct, few studies have examined the relationship between renal function and SBI, and these may have been limited by the inaccuracy of creatinine as a renal function marker. A cross-sectional study was performed among older adults in the Cardiovascular Health Study to examine associations between SBI and two serum markers of renal function: Serum creatinine (SCr) and cystatin C (CysC). Patients had cranial magnetic resonance imaging and renal markers measured in 1992 to 1993. Logistic regression was used to estimate the associations between renal function (estimated by 1/SCr and 1/CysC) and SBI, controlling for potential confounding factors. SBI were present in 789 (28.7%) of 2784 participants. A linear association with SBI was observed for 1/CysC (per 1-SD decrement; odds ratio [OR] 1.20; 95% confidence interval [CI] 1.09 to 1.32; P < 0.001) but not for 1/SCr (OR 1.08; 95% CI 0.98 to 1.19; P = 0.14), for which a quadratic U-shaped association was suggested (P = 0.004). In a model with both markers, 1/CysC was linearly associated with SBI (OR 1.26; P < 0.001), whereas 1/SCr was not (OR 1.06; P = 0.3). The prevalence of SBI was directly associated with quintile of CysC, whereas the association between SCr and SBI was U-shaped, with greater prevalence at high and low levels. Compared with creatinine, CysC, a novel marker of renal function, has a stronger and more direct association with SBI in the elderly.
10aAge Factors10aAged10aAged, 80 and over10aBiomarkers10aBrain Infarction10aConfidence Intervals10aCreatinine10aCross-Sectional Studies10aCystatin C10aCystatins10aDisease Progression10aFemale10aGeriatric Assessment10aHumans10aIncidence10aIschemic Attack, Transient10aMagnetic Resonance Imaging10aMale10aOdds Ratio10aPredictive Value of Tests10aPrognosis10aRisk Assessment10aSensitivity and Specificity10aSeverity of Illness Index10aSex Factors10aSurvival Analysis1 aSeliger, Stephen, L1 aLongstreth, W T1 aKatz, Ronit1 aManolio, Teri1 aFried, Linda, F1 aShlipak, Michael1 aStehman-Breen, Catherine, O1 aNewman, Anne1 aSarnak, Mark1 aGillen, Daniel, L1 aBleyer, Anthony1 aSiscovick, David, S uhttps://chs-nhlbi.org/node/86202953nas a2200457 4500008004100000022001400041245010600055210006900161260001300230300001000243490000700253520169200260653002701952653000901979653001701988653001502005653001502020653001402035653001102049653000802060653001102068653002002079653002602099653001802125653002502143653000902168653001702177653003002194100002002224700002402244700002902268700002402297700002102321700001702342700001802359700002102377700002202398700002002420700002002440856003502460 2006 eng d a1079-500600aKidney function predicts the rate of bone loss in older individuals: the Cardiovascular Health Study.0 aKidney function predicts the rate of bone loss in older individu c2006 Jul a743-80 v613 aBACKGROUND: Results of cross-sectional analyses of the association of kidney function with bone mineral density (BMD) have been conflicting. We examined the association of cystatin-C, a new marker of kidney function that is unrelated to lean mass, with initial and follow-up BMD, in an ancillary study of the Cardiovascular Health Study, a population-based cohort of individuals > or = 65 years old.
METHODS: Two years after measurement of cystatin-C and other covariates, the first BMD was measured in Pittsburgh, Pennsylvania and Davis, California, by using dual energy x-ray absorptiometry. Follow-up BMD was measured in Pittsburgh 4 years later. Associations of cystatin-C with initial BMD and the change in BMD (%/y) at the hip were examined with linear regression. Analyses were conducted separately for men and women.
RESULTS: In 1519 participants who had cystatin-C and initial BMD assessed, 614 had follow-up BMD. The percent annual change in BMD at the total hip by cystatin-C quartiles was -0.24, -0.13, -0.40, and -0.66%/y (first to fourth quartile) in women and -0.02, -0.30, -0.18, and -0.94%/y in men. After adjusting for potential confounders, cystatin-C was marginally associated with initial BMD in men but not women. Cystatin-C was associated with bone loss in men; after adjustment for weight loss, cystatin-C was not associated with bone loss in women.
CONCLUSION: Kidney dysfunction, as assessed by cystatin-C, is associated with a more rapid loss of BMD at the hip, especially in men. Further studies are needed to confirm these findings and to determine whether this loss leads to an elevated risk of fracture.
10aAbsorptiometry, Photon10aAged10aBone Density10aCreatinine10aCystatin C10aCystatins10aFemale10aHip10aHumans10aKidney Diseases10aKidney Function Tests10aLinear Models10aLongitudinal Studies10aMale10aOsteoporosis10aPredictive Value of Tests1 aFried, Linda, F1 aShlipak, Michael, G1 aStehman-Breen, Catherine1 aMittalhenkle, Anuja1 aSeliger, Stephen1 aSarnak, Mark1 aRobbins, John1 aSiscovick, David1 aHarris, Tamara, B1 aNewman, Anne, B1 aCauley, Jane, A uhttps://chs-nhlbi.org/node/90802943nas a2200457 4500008004100000022001400041245007900055210006900134260001300203300001000216490000700226520171800233653000901951653002201960653001501982653001401997653001102011653001802022653001102040653001102051653002802062653002502090653000902115653001702124653002402141653001702165653001602182100002002198700002402218700002402242700002102266700002202287700002902309700001702338700002102355700001902376700001702395700002002412700001802432856003502450 2007 eng d a1046-667300aAssociation of kidney function with incident hip fracture in older adults.0 aAssociation of kidney function with incident hip fracture in old c2007 Jan a282-60 v183 aKidney dysfunction is associated with bone loss, and patients with ESRD have an increased risk for hip fracture. However, the association of mild to moderate kidney disease with hip fracture has not been studied previously. The association of kidney function with incident hip fracture was examined among participants in the Cardiovascular Health Study, a community-based cohort of older individuals. The primary measure of kidney function was serum cystatin C, a measure that does not depend on lean mass. Hip fractures were identified using International Classification of Diseases, Ninth Revision codes for hospitalizations. A total of 4699 individuals had cystatin C measured in 1992 to 1993 and did not have a hip fracture before cystatin C measurement. The association of kidney function with hip fracture was analyzed with Cox proportional hazards models. Analyses were conducted separately for men and women. After a mean follow-up of 7.1 yr, 195 incident hip fractures occurred in women and 79 occurred in men. Higher cystatin C levels were associated with a higher risk for fracture in women (hazard ratio [HR] 1.26; 95% confidence interval [CI] 1.14 to 1.38 per SD) and in men (HR 1.27; 95% CI 1.11 to 1.46). After multivariable adjustment, higher cystatin C levels were significantly associated with hip fracture in women (HR 1.16; 95% CI 1.01, 1.33) but not in men (HR 1.14; 95% CI 0.86 to 1.52), although the magnitude of the association was similar. Kidney dysfunction, as assessed by cystatin C, is associated with an increased risk for hip fracture. Further studies are needed to evaluate potential mediators of this relationship and to assess whether interventions can decrease this risk.
10aAged10aAged, 80 and over10aCystatin C10aCystatins10aFemale10aHip Fractures10aHumans10aKidney10aKidney Failure, Chronic10aLongitudinal Studies10aMale10aOsteoporosis10aProspective Studies10aRisk Factors10aSex Factors1 aFried, Linda, F1 aBiggs, Mary, Louise1 aShlipak, Michael, G1 aSeliger, Stephen1 aKestenbaum, Bryan1 aStehman-Breen, Catherine1 aSarnak, Mark1 aSiscovick, David1 aHarris, Tamara1 aCauley, Jane1 aNewman, Anne, B1 aRobbins, John uhttps://chs-nhlbi.org/node/93302609nas a2200445 4500008004100000022001400041245007800055210006900133260000900202300001100211490000700222520142700229653000901656653002201665653001501687653002301702653002101725653001501746653002201761653001601783653001101799653002201810653001101832653002401843653001801867653002001885653000901905653001501914653003301929653001701962653001501979100002001994700001602014700001802030700001702048700002402065700001802089700002002107856003602127 2009 eng d a1421-967000aChange in cardiovascular risk factors with progression of kidney disease.0 aChange in cardiovascular risk factors with progression of kidney c2009 a334-410 v293 aBACKGROUND: Prior studies evaluating the relationship of kidney disease with cardiovascular risk factors have been limited by their cross-sectional design. We evaluated the change in lipids, inflammatory and procoagulant biomarkers with decline in kidney function in a nested case-cohort study in the Cardiovascular Health Study, a community-based study of adults aged >65 years.
METHODS: Individuals with an increase in serum creatinine >or=0.3 mg/dl (baseline to 3 years later, n = 207) were matched to controls of similar age, race, gender, diabetes and baseline serum creatinine, but whose change in creatinine was <0.3 mg/dl. Baseline and change in risk factors were analyzed with conditional logistic regression.
RESULTS: Changes in C-reactive protein were similar. In contrast, cases had larger increases in fibrinogen (OR 1.38 per standard deviation, 95% confidence interval 1.08-1.76) and factor VIII [1.38 (1.10-1.72)] and larger decreases in HDL [OR 0.80 (0.64, 1.00)]. Change in interleukin-6 was greater in cases than controls, but this did not persist after multivariate adjustment. However, in linear regression, change in interleukin-6 was correlated with change in creatinine.
CONCLUSION: Cardiovascular risk factors and kidney function may change concurrently. This could lead to an increased risk of cardiovascular disease as kidney function worsens.
10aAged10aAged, 80 and over10aBiomarkers10aC-Reactive Protein10aCholesterol, HDL10aCreatinine10aDiabetes Mellitus10aFactor VIII10aFemale10aFollow-Up Studies10aHumans10aHypertension, Renal10aInterleukin-610aLogistic Models10aMale10aPrevalence10aRenal Insufficiency, Chronic10aRisk Factors10aVasculitis1 aFried, Linda, F1 aKatz, Ronit1 aCushman, Mary1 aSarnak, Mark1 aShlipak, Michael, G1 aKuller, Lewis1 aNewman, Anne, B uhttps://chs-nhlbi.org/node/106103209nas a2200769 4500008004100000022001400041245008800055210006900143260001300212300001000225490000700235520104200242653002301284653001901307653002201326653003401348653003101382653001101413653001101424653002801435653002701463653001701490653001601507653003601523653001501559653001501574100001901589700002201608700001901630700002001649700001601669700001201685700001601697700002401713700002201737700002201759700002101781700001901802700001901821700002101840700002001861700002001881700002301901700002201924700002001946700002301966700001901989700001702008700002102025700002402046700001702070700002102087700002402108700001902132700002602151700002802177700002302205700002302228700002102251700002002272700002002292700002802312700001802340700002402358700002102382856003602403 2009 eng d a1546-171800aMultiple loci associated with indices of renal function and chronic kidney disease.0 aMultiple loci associated with indices of renal function and chro c2009 Jun a712-70 v413 aChronic kidney disease (CKD) has a heritable component and is an important global public health problem because of its high prevalence and morbidity. We conducted genome-wide association studies (GWAS) to identify susceptibility loci for glomerular filtration rate, estimated by serum creatinine (eGFRcrea) and cystatin C (eGFRcys), and CKD (eGFRcrea < 60 ml/min/1.73 m(2)) in European-ancestry participants of four population-based cohorts (ARIC, CHS, FHS, RS; n = 19,877; 2,388 CKD cases), and tested for replication in 21,466 participants (1,932 CKD cases). We identified significant SNP associations (P < 5 × 10(-8)) with CKD at the UMOD locus, with eGFRcrea at UMOD, SHROOM3 and GATM-SPATA5L1, and with eGFRcys at CST and STC1. UMOD encodes the most common protein in human urine, Tamm-Horsfall protein, and rare mutations in UMOD cause mendelian forms of kidney disease. Our findings provide new insights into CKD pathogenesis and underscore the importance of common genetic variants influencing renal function and disease.
10aChromosome Mapping10aCohort Studies10aGenetic Variation10aGenome-Wide Association Study10aGlomerular Filtration Rate10aHumans10aKidney10aKidney Failure, Chronic10aMeta-Analysis as Topic10aMucoproteins10aNetherlands10aPolymorphism, Single Nucleotide10aPrevalence10aUromodulin1 aKöttgen, Anna1 aGlazer, Nicole, L1 aDehghan, Abbas1 aHwang, Shih-Jen1 aKatz, Ronit1 aLi, Man1 aYang, Qiong1 aGudnason, Vilmundur1 aLauner, Lenore, J1 aHarris, Tamara, B1 aSmith, Albert, V1 aArking, Dan, E1 aAstor, Brad, C1 aBoerwinkle, Eric1 aEhret, Georg, B1 aRuczinski, Ingo1 aScharpf, Robert, B1 aChen, Yii-Der Ida1 ade Boer, Ian, H1 aHaritunians, Talin1 aLumley, Thomas1 aSarnak, Mark1 aSiscovick, David1 aBenjamin, Emelia, J1 aLevy, Daniel1 aUpadhyay, Ashish1 aAulchenko, Yurii, S1 aHofman, Albert1 aRivadeneira, Fernando1 aUitterlinden, André, G1 aDuijn, Cornelia, M1 aChasman, Daniel, I1 aParé, Guillaume1 aRidker, Paul, M1 aKao, Linda, W H1 aWitteman, Jacqueline, C1 aCoresh, Josef1 aShlipak, Michael, G1 aFox, Caroline, S uhttps://chs-nhlbi.org/node/109902654nas a2200373 4500008004100000022001400041245007900055210006900134260001600203300001200219490000800231520161700239653000901856653001501865653001101880653003101891653001101922653002601933653002501959653000901984653001901993653002402012653001702036100003002053700001602083700002502099700002502124700001702149700001702166700001802183700002102201700002202222856003602244 2009 eng d a1538-367900aPhysical activity and rapid decline in kidney function among older adults.0 aPhysical activity and rapid decline in kidney function among old c2009 Dec 14 a2116-230 v1693 aBACKGROUND: Habitual physical activity (PA) has both physiologic and metabolic effects that may moderate the risk of kidney function decline. We tested the hypothesis that higher levels of PA are associated with a lower risk of kidney function decline using longitudinal data from a large cohort of older adults.
METHODS: We studied 4011 ambulatory participants aged 65 or older from the Cardiovascular Health Study (CHS) who completed at least 2 measurements of kidney function over 7 years. We calculated a PA score (range, 2-8) by summing kilocalories expended per week (ordinal score of 1-5 from quintiles of kilocalories per week) and walking pace (ordinal score for categories of <2, 2-3, and >3 mph). Rapid decline in kidney function decline (RDKF) was defined by loss of more than 3.0 mL/min/1.73 m(2) per year in glomerular filtration rate, which we estimated by using longitudinal measurements of cystatin C levels.
RESULTS: A total of 958 participants had RDKF (23.9%; 4.1 events per 100 person-years). The estimated risk of RDKF was 16% in the highest PA group (score of 8) and 30% in the lowest PA group (score of 2). After multivariate adjustment, we found that the 2 highest PA groups (scores of 7-8) were associated with a 28% lower risk of RDKF (95% confidence interval, 21%-41% lower risk) than the 2 lowest PA groups (score of 2-3). Greater kilocalories of leisure-time PA and walking pace were also each associated with a lower incidence of RDKF.
CONCLUSION: Higher levels of PA are associated with a lower risk of RDKF among older adults.
10aAged10aCystatin C10aFemale10aGlomerular Filtration Rate10aHumans10aKidney Function Tests10aLongitudinal Studies10aMale10aMotor Activity10aRenal Insufficiency10aTime Factors1 aRobinson-Cohen, Cassianne1 aKatz, Ronit1 aMozaffarian, Dariush1 aDalrymple, Lorien, S1 ade Boer, Ian1 aSarnak, Mark1 aShlipak, Mike1 aSiscovick, David1 aKestenbaum, Bryan uhttps://chs-nhlbi.org/node/114802802nas a2200469 4500008004100000022001400041245009700055210006900152260000900221300001000230490000700240520155000247653000901797653002801806653001501834653001501849653002401864653001101888653001501899653003101914653001101945653001101956653002001967653000901987653001601996653002202012653001702034653002202051100002302073700001602096700002102112700001602133700001602149700001702165700002502182700001602207700002202223700001602245700001702261700001802278856003602296 2011 eng d a1421-967000aKidney function decline in the elderly: impact of lipoprotein-associated phospholipase A(2).0 aKidney function decline in the elderly impact of lipoproteinasso c2011 a512-80 v343 aBACKGROUND: Whether lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) levels are associated with kidney function decline has not been well studied.
METHODS: We investigated associations of Lp-PLA(2) antigen and activity with kidney function decline and rapid decline over 5.7 years in the Cardiovascular Health Study (n = 4,359). We estimated kidney function by cystatin C (eGFRcys) in repeated measures, and defined rapid decline as ≥3 ml/min/1.73 m(2) per year. We stratified by baseline preserved GFR (≥60 ml/min/1.73 m(2)).
RESULTS: Mean age was 72 ± 5 years. Average eGFRcys decline was -1.79 ml/min/1.73 m(2) (SD = 2.60) per year. Among persons with preserved GFR, compared to the lowest quartile of Lp-PLA(2) antigen, eGFRcys decline was faster among persons in the second, β -0.31 (95% CI -0.52, -0.10), third -0.19 (-0.41, 0.02) and fourth quartiles -0.26 (-0.48, -0.04) after full adjustment. Persons in the highest quartile of Lp-PLA(2) antigen had increased odds of rapid decline 1.34 (1.03, 1.75), compared to the lowest. There was no significant association between levels of Lp-PLA(2) activity and eGFRcys decline or rapid decline. Associations were not statistically significant among persons with low eGFR (<60 ml/min/1.73 m(2)) at baseline.
CONCLUSION: Higher levels of Lp-PLA(2) antigen but not activity were significantly associated with faster rates of kidney function decline. These findings may suggest a novel vascular pathway for kidney disease progression.
10aAged10aCardiovascular Diseases10aCreatinine10aCystatin C10aDisease Progression10aFemale10aGeriatrics10aGlomerular Filtration Rate10aHumans10aKidney10aKidney Diseases10aMale10aMiddle Aged10aPhospholipases A210aRisk Factors10aTreatment Outcome1 aPeralta, Carmen, A1 aKatz, Ronit1 aShlipak, Michael1 aDubin, Ruth1 aDeBoer, Ian1 aJenny, Nancy1 aFitzpatrick, Annette1 aKoro, Carol1 aKestenbaum, Bryan1 aIx, Joachim1 aSarnak, Mark1 aCushman, Mary uhttps://chs-nhlbi.org/node/134902980nas a2200409 4500008004100000022001400041245012500055210006900180260001300249300001000262490000800272520179200280653000902072653001102081653003002092653002102122653001102143653003402154653002502188653000902213653003302222653001702255653002002272100002102292700001902313700002102332700001602353700001602369700002202385700002002407700001702427700002402444700002402468700002102492700002102513856003602534 2013 eng d a1879-148400aFibroblast growth factor 23, left ventricular mass, and left ventricular hypertrophy in community-dwelling older adults.0 aFibroblast growth factor 23 left ventricular mass and left ventr c2013 Nov a114-90 v2313 aOBJECTIVES: In chronic kidney disease (CKD), high FGF23 concentrations are associated with left ventricular hypertrophy (LVH), cardiovascular events, and death. The associations of FGF23 with left ventricular mass (LVM) and LVH in the general population and the influence of CKD remains uncertain.
METHODS: C-terminal plasma FGF23 concentrations were measured, and LVM and LVH evaluated by echocardiogram among 2255 individuals ≥65 years in the Cardiovascular Health Study. Linear regression analysis adjusting for demographics, cardiovascular, and kidney related risk factors examined the associations of FGF23 concentrations with LVM. Analyses were stratified by CKD status and adjusted linear and logistic regression analysis explored the associations of FGF23 with LVM and LVH.
RESULTS: Among the entire cohort, higher FGF23 concentrations were associated with greater LVM in adjusted analyses (β = 6.71 [95% CI 4.35-9.01] g per doubling of FGF23). 32% (n = 624) had CKD (eGFR <60 mL/min/1.73 m(2) and/or urine albumin-to-creatinine ratio >30 mg/g). Associations were stronger among participants with CKD (p interaction = 0.006): LVM β = 9.71 [95% CI 5.86-13.56] g per doubling of FGF23 compared to those without CKD (β = 3.44 [95% CI 0.77, 6.11] g per doubling of FGF23). While there was no significant interaction between FGF23 and CKD for LVH (p interaction = 0.25), the OR (1.46 95% CI [1.20-1.77]) in the CKD group was statistically significant and of larger magnitude than the OR for in the no CKD group (1.12 [95% CI 0.97-1.48]).
CONCLUSION: In a large cohort of older community-dwelling adults, higher FGF23 concentrations were associated with greater LVM and LVH with stronger relationships in participants with CKD.
10aAged10aFemale10aFibroblast Growth Factors10aHeart Ventricles10aHumans10aHypertrophy, Left Ventricular10aLongitudinal Studies10aMale10aRenal Insufficiency, Chronic10aRisk Factors10aUltrasonography1 aJovanovich, Anna1 aIx, Joachim, H1 aGottdiener, John1 aMcFann, Kim1 aKatz, Ronit1 aKestenbaum, Bryan1 ade Boer, Ian, H1 aSarnak, Mark1 aShlipak, Michael, G1 aMukamal, Kenneth, J1 aSiscovick, David1 aChonchol, Michel uhttps://chs-nhlbi.org/node/737903861nas a2200565 4500008004100000022001400041245010700055210006900162260001500231300001100246490000700257520230700264653001602571653000902587653001002596653001502606653001502621653002402636653001102660653003102671653001102702653001402713653001102727653001802738653002502756653000902781653003102790653002202821653003002843653001402873653003202887653002402919653003302943653001702976653001702993653001503010653001803025653001803043100001803061700001603079700002203095700001703117700002703134700002203161700001703183700001703200700002103217700002103238856003603259 2015 eng d a1555-905X00aNT-proBNP and troponin T and risk of rapid kidney function decline and incident CKD in elderly adults.0 aNTproBNP and troponin T and risk of rapid kidney function declin c2015 Feb 6 a205-140 v103 aBACKGROUND AND OBJECTIVES: Elevations in N-terminal pro-B-type natriuretic peptide and high-sensitivity troponin T are associated with poor cardiovascular outcomes. Whether elevations in these cardiac biomarkers are associated with decline in kidney function was evaluated.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: N-terminal pro-B-type natriuretic peptide and troponin T were measured at baseline in 3752 participants free of heart failure in the Cardiovascular Health Study. eGFR was determined from the Chronic Kidney Disease Epidemiology Collaboration equation using serum cystatin C. Rapid decline in kidney function was defined as decline in serum cystatin C eGFR≥30%, and incident CKD was defined as the onset of serum cystatin C eGFR<60 among those without CKD at baseline (n=2786). Cox regression models were used to examine the associations of each biomarker with kidney function decline adjusting for demographics, baseline serum cystatin C eGFR, diabetes, and other CKD risk factors.
RESULTS: In total, 503 participants had rapid decline in serum cystatin C eGFR over a mean follow-up time of 6.41 (1.81) years, and 685 participants developed incident CKD over a mean follow-up time of 6.41 (1.74) years. Participants in the highest quartile of N-terminal pro-B-type natriuretic peptide (>237 pg/ml) had an 67% higher risk of rapid decline and 38% higher adjusted risk of incident CKD compared with participants in the lowest quartile (adjusted hazard ratio for serum cystatin C eGFR rapid decline, 1.67; 95% confidence interval, 1.25 to 2.23; hazard ratio for incident CKD, 1.38; 95% confidence interval, 1.08 to 1.76). Participants in the highest category of troponin T (>10.58 pg/ml) had 80% greater risk of rapid decline compared with participants in the lowest category (adjusted hazard ratio, 1.80; 95% confidence interval, 1.35 to 2.40). The association of troponin T with incident CKD was not statistically significant (hazard ratio, 1.17; 95% confidence interval, 0.92 to 1.50).
CONCLUSIONS: Elevated N-terminal pro-B-type natriuretic peptide and troponin T are associated with rapid decline of kidney function and incident CKD. Additional studies are needed to evaluate the mechanisms that may explain this association.
10aAge Factors10aAged10aAging10aBiomarkers10aCystatin C10aDisease Progression10aFemale10aGlomerular Filtration Rate10aHumans10aIncidence10aKidney10aLinear Models10aLongitudinal Studies10aMale10aNatriuretic Peptide, Brain10aPeptide Fragments10aPredictive Value of Tests10aPrognosis10aProportional Hazards Models10aProspective Studies10aRenal Insufficiency, Chronic10aRisk Factors10aTime Factors10aTroponin T10aUnited States10aUp-Regulation1 aBansal, Nisha1 aKatz, Ronit1 aDalrymple, Lorien1 ade Boer, Ian1 aDeFilippi, Christopher1 aKestenbaum, Bryan1 aPark, Meyeon1 aSarnak, Mark1 aSeliger, Stephen1 aShlipak, Michael uhttps://chs-nhlbi.org/node/666103249nas a2200385 4500008004100000022001400041245014700055210006900202260001600271520204100287100001902328700001902347700003002366700002602396700003102422700001902453700002102472700002102493700002502514700001702539700002102556700002502577700001602602700002302618700002102641700002002662700001902682700001902701700002202720700001802742700001802760700002802778700002102806856003602827 2020 eng d a1523-175500aA systematic review and participant-level meta-analysis found little association of retinal microvascular caliber and reduced kidney function.0 asystematic review and participantlevel metaanalysis found little c2020 Aug 153 aPreviously, variation in retinal vascular caliber has been reported in association with chronic kidney disease (CKD) but findings remain inconsistent. To help clarify this we conducted individual participant data meta-analysis and aggregate data meta-analysis on summary estimates to evaluate cross-sectional associations between retinal vascular caliber and CKD. A systematic review was performed using Medline and EMBASE for articles published until October 2018. The aggregate analysis used a two-stage approach combining summary estimates from eleven studies (44,803 patients) while the individual participant analysis used a one-stage approach combining raw data from nine studies (33,222 patients). CKD stages 3-5 was defined as an estimated glomerular filtration rate under 60 mL/min/1.73m. Retinal arteriolar and venular caliber (central retinal arteriolar and venular equivalent) were assessed from retinal photographs using computer-assisted methods. Logistic regression estimated relative risk of CKD stages 3-5 associated with a 20 μm decrease (approximately one standard deviation) in central retinal arteriolar and venular equivalent. Prevalence of CKD stages 3-5 was 11.2 % of 33,222 and 11.3 % of 44,803 patients in the individual participant and aggregate data analysis, respectively. No significant associations were detected in adjusted analyses between central retinal arteriolar and venular equivalent and CKD stages 3-5 in the aggregate analysis for central retinal arteriolar relative risk (0.98, 95% confidence interval 0.94-1.03); venular equivalent (0.99, 0.95- 1.04) or individual participant central retinal arteriolar (0.99, 0.95-1.04) or venular equivalent (1.01, 0.97-1.05). Thus, meta-analysis provided little evidence to suggest that cross sectional direct measurements of retinal vascular caliber was associated with CKD stages 3-5 in the general population. Hence, meta-analyses of longitudinal studies evaluating the association between retinal parameters and CKD stages 3-5 may be warranted.
1 aLye, Weng, Kit1 aPaterson, Euan1 aPatterson, Christopher, C1 aMaxwell, Alexander, P1 aAbdul, Riswana, Banu Binte1 aTai, Shyong, E1 aCheng, Ching, Yu1 aKayama, Takamasa1 aYamashita, Hidetoshi1 aSarnak, Mark1 aShlipak, Michael1 aMatsushita, Kunihiro1 aMutlu, Unal1 aIkram, Mohammad, A1 aKlaver, Caroline1 aKifley, Annette1 aMitchell, Paul1 aMyers, Chelsea1 aKlein, Barbara, E1 aKlein, Ronald1 aWong, Tien, Y1 aSabanayagam, Charumathi1 aMcKay, Gareth, J uhttps://chs-nhlbi.org/node/8628