The prevalence of hematologic and metabolic abnormalities during chronic kidney disease stages in different ethnic groups

We conducted an observational cross-sectional study to determine if the prevalence of hematologic and metabolic abnormalities in chronic kidney disease (CKD) varied in different ethnic groups. We used a CKD provincial database where a complete data set at the time of registration was available as well as an estimated glomerular filtration rate (eGFR), which showed using the abbreviated MDRD formula that the patients had CKD of stages 3–5. We included patients with self-reported race of Caucasian, Oriental Asian, or South Asian. Primary outcomes were the prevalence of at least one of the following: anemia, hypocalcemia, hyperphosphatemia, hyperparathyroidism, hypoalbuminemia, and three or more laboratory abnormalities. All definitions were consistent with K/DOQI guidelines. When compared with Caucasians, Oriental Asians and South Asians had a higher prevalence of many of the metabolic abnormalities during most stages of CKD and were more likely to have any abnormality at all levels of eGFR. The prevalence of three or more laboratory abnormalities was higher in Oriental Asians at all stages and in South Asians at some levels of eGFR. These results were unchanged or exaggerated when controlled for age, gender, diabetes, and a primary diagnosis of renal disease. Hence, it appears that South Asians and Oriental Asians have more laboratory abnormalities compared with Caucasians at most levels of eGFR

KONKURENTNOST TURISTIČKE DESTINACIJE – IZMEĐU DVIJU ZASTAVA

The study aims to provide a better understanding of destination competitiveness and elements that affect competitive position of a tourism destination. The research is design as a comparative study of Slovenia and Serbia. For analysing a competitiveness of mentioned destinations, the Integrated model of destination competitiveness was used. The results showed that both destinations are considered to be more competitive in its natural, cultural, and created resources, but less competitive in the destination management and, according to the Integrated model, demand conditions. Based on these findings, relevant proposals are made in order to improve competitive positions of destinations.Cilj rada je ponuditi bolje razumijevanje konkurentnosti destinacije i elemenata koji utječu na konkurentnu poziciju turističke destinacije. Istraživanje je osmišljeno kao komparativna studija Slovenije i Srbije. Za analizu konkurentnosti spomenutih destinacija korišten je integrirani model konkurentnosti destinacije. Rezultati su pokazali da se obje destinacije smatraju konkurentnijima u njihovim prirodnim, kulturnim i stvorenim resursima, dok su znatno manje konkurentne po menadžmentu destinacije i, sudeći po integriranom modelu, po uvjetima potražnje. Na osnovu ovih nalaza, daju se relevantni prijedlozi kako bi se poboljšale konkurentne pozicije destinacija

Supplementary Material for: The Association between Biomarker Profiles, Etiology of Chronic Kidney Disease, and Mortality

<p><b><i>Background:</i></b> Prognosis in chronic kidney disease (CKD) for adverse outcomes differs substantially based on the etiology of CKD. We examined whether the biomarker profile differed based on CKD etiology and whether they were associated with mortality. <b><i>Methods:</i></b> Prospective observational study of 1,157 patients, 663 with diabetic kidney disease (DKD), 273 with glomerulonephritis (GN), and 221 with cystic/interstitial disease (polycystic kidney disease, pyelonephritis or chronic tubulointerstitial nephritis [PCK/TIN]) were identified in the Canadian Study of Prediction of Dialysis, Death and Interim Cardiovascular events over Time cohort. The outcome of interest was mortality before commencing dialysis. The biomarker profile consisted of N-terminal pro-brain natriuretic peptide (NT-proBNP), troponin I (TnI), asymmetric dimethylarginine (ADMA), interleukin (IL)-6, high sensitivity C-reactive protein, fibroblast growth factor-23 (FGF23), transforming growth factor-beta, 25-hydroxylvitamin D, and cystatin C (CysC). <b><i>Results:</i></b> The mean estimated glomerular filtration rate was 27 mL/min/1.73 m² and median follow-up time was 44 months. Mortality before dialysis commencement was the greatest in DKD (20%), followed by PCK/TIN (13%), and was least in those GN (8%). The majority of deaths were cardiovascular in nature, 17, 9, and 5.5% for DKD, PCK/TIN, GN, respectively. Those with DKD had higher hazard for mortality, unadjusted (hazard ratio [HR] 2.7, 95% CI 1.7-4.3) and adjusted (HR 1.7, 95% CI 1.1-2.8). The biomarker profiles associated with mortality differed significantly by CKD etiology as follows: DKD was associated with CysC (HR 1.3, 95% CI 1.0-1.6), ADMA (HR 1.3, 95% CI 1.1-1.6), and NT-proBNP (HR 1.7, 95% CI 1.4-2.1), GN was associated with FGF23 (HR 1.8, 95% CI 1.1-2.8), TnI (HR 3.6, 95% CI 1.3-9.5), and transforming growth factor-beta (HR 0.6, 95% CI 0.4-0.9) and PCK/TIN was associated with ADMA (HR 1.5, 95% CI 1.3-1.8) and IL-6 (HR 2.1, 95% CI 1.5-3.1). <b><i>Conclusions:</i></b> Biomarkers profiles differ according to the etiology of CKD and are associated with mortality.</p

PowerPoint Slides for: The Association between Biomarker Profiles, Etiology of Chronic Kidney Disease, and Mortality

<p><b><i>Background:</i></b> Prognosis in chronic kidney disease (CKD) for adverse outcomes differs substantially based on the etiology of CKD. We examined whether the biomarker profile differed based on CKD etiology and whether they were associated with mortality. <b><i>Methods:</i></b> Prospective observational study of 1,157 patients, 663 with diabetic kidney disease (DKD), 273 with glomerulonephritis (GN), and 221 with cystic/interstitial disease (polycystic kidney disease, pyelonephritis or chronic tubulointerstitial nephritis [PCK/TIN]) were identified in the Canadian Study of Prediction of Dialysis, Death and Interim Cardiovascular events over Time cohort. The outcome of interest was mortality before commencing dialysis. The biomarker profile consisted of N-terminal pro-brain natriuretic peptide (NT-proBNP), troponin I (TnI), asymmetric dimethylarginine (ADMA), interleukin (IL)-6, high sensitivity C-reactive protein, fibroblast growth factor-23 (FGF23), transforming growth factor-beta, 25-hydroxylvitamin D, and cystatin C (CysC). <b><i>Results:</i></b> The mean estimated glomerular filtration rate was 27 mL/min/1.73 m² and median follow-up time was 44 months. Mortality before dialysis commencement was the greatest in DKD (20%), followed by PCK/TIN (13%), and was least in those GN (8%). The majority of deaths were cardiovascular in nature, 17, 9, and 5.5% for DKD, PCK/TIN, GN, respectively. Those with DKD had higher hazard for mortality, unadjusted (hazard ratio [HR] 2.7, 95% CI 1.7-4.3) and adjusted (HR 1.7, 95% CI 1.1-2.8). The biomarker profiles associated with mortality differed significantly by CKD etiology as follows: DKD was associated with CysC (HR 1.3, 95% CI 1.0-1.6), ADMA (HR 1.3, 95% CI 1.1-1.6), and NT-proBNP (HR 1.7, 95% CI 1.4-2.1), GN was associated with FGF23 (HR 1.8, 95% CI 1.1-2.8), TnI (HR 3.6, 95% CI 1.3-9.5), and transforming growth factor-beta (HR 0.6, 95% CI 0.4-0.9) and PCK/TIN was associated with ADMA (HR 1.5, 95% CI 1.3-1.8) and IL-6 (HR 2.1, 95% CI 1.5-3.1). <b><i>Conclusions:</i></b> Biomarkers profiles differ according to the etiology of CKD and are associated with mortality.</p

Change in GFR and Subsequent Mortality: Meta-Analysis of 32 Cohorts in the CKD Prognosis Consortium

Background: Change in estimated GFR (eGFR) is frequently used to track CKD progression in clinical practice, trials and cohort studies but its association with mortality has not been studied extensively. Methods: Change in eGFR was estimated as % change from the rst to last eGFR (CKD-EPI creatinine) in a 2-year baseline period. We modeled the hazard ratios (HRs) of subsequent mortality as a spline function of %change in eGFR after adjusting for age, sex, race, rst eGFR, and co-morbid conditions. We used random effects meta-analyses to combine results strati ed by rst baseline eGFR (<60 60) across studies. Results: Mortality follow-up of 910,660 participants from 32 cohorts for a mean of 4.2 years after the 2-year baseline period showed 91,398 deaths for baseline eGFR <60 (n=333,722) and 45,063 deaths for baseline eGFR 60 (n=576,938). Change in eGFR had a non-linear association with mortality (Figure for eGFR<60). A decline in eGFR was consistently associated with higher subsequent mortality risk (adjusted HR for -30% vs. 0% change in eGFR were: 1.8 at eGFR <60; and 1.5 at eGFR 60; p<0.001). Similar results were obtained for a 1- or 3-year change in eGFR. Hazards ratios were largely similar for those with eGFR 60 or when strati ed by ACR levels. Conclusions: Declines in eGFR are strongly and consistently associated with subsequent risk of mortality adjusted for the rst eGFR and covariates. These ndings support using smaller changes than -57% (equivalent to doubling of serum creatinine) in clinical research

Change in GFR and Subsequent Mortality: Meta-Analysis of 32 Cohorts in the CKD Prognosis Consortium

Background: Change in estimated GFR (eGFR) is frequently used to track CKD progression in clinical practice, trials and cohort studies but its association with mortality has not been studied extensively. Methods: Change in eGFR was estimated as % change from the rst to last eGFR (CKD-EPI creatinine) in a 2-year baseline period. We modeled the hazard ratios (HRs) of subsequent mortality as a spline function of %change in eGFR after adjusting for age, sex, race, rst eGFR, and co-morbid conditions. We used random effects meta-analyses to combine results strati ed by rst baseline eGFR (<60 60) across studies. Results: Mortality follow-up of 910,660 participants from 32 cohorts for a mean of 4.2 years after the 2-year baseline period showed 91,398 deaths for baseline eGFR <60 (n=333,722) and 45,063 deaths for baseline eGFR 60 (n=576,938). Change in eGFR had a non-linear association with mortality (Figure for eGFR<60). A decline in eGFR was consistently associated with higher subsequent mortality risk (adjusted HR for -30% vs. 0% change in eGFR were: 1.8 at eGFR <60; and 1.5 at eGFR 60; p<0.001). Similar results were obtained for a 1- or 3-year change in eGFR. Hazards ratios were largely similar for those with eGFR 60 or when strati ed by ACR levels. Conclusions: Declines in eGFR are strongly and consistently associated with subsequent risk of mortality adjusted for the rst eGFR and covariates. These ndings support using smaller changes than -57% (equivalent to doubling of serum creatinine) in clinical research

DECLINE IN ESTIMATED GLOMERULAR FILTRATION RATE AND SUBSEQUENT RISK OF MORTALITY: A META-ANALYSIS OF 35 COHORTS IN THE CKD PROGNOSIS CONSORTIUM

Introduction and Aims: Change in estimated GFR (eGFR) is frequently used to track CKD progression in clinical practice, trials and cohort studies but its association with mortality has not been studied extensively. Methods: Change in eGFR was estimated as % change from the first to last eGFR (CKD-EPI creatinine) in a 2-year baseline period.We modeled the hazard ratios (HRs) of subsequent mortality as a spline function of % change in eGFR after adjusting for age, sex, race, first eGFR, and co-morbid conditions.We used random effects meta-analyses to combine results stratified by first baseline eGFR (<60 & ≥60) across studies. Results: Mortality follow-up of 1,597,723 participants from 32 cohorts for a mean of 3.7 years after the 2-year baseline period showed 101,120 deaths for baseline eGFR <60 (n=395,394) and 57,472 deaths for baseline eGFR ≥60 (n=1,202,329). Change in eGFR had a non-linear association with mortality (Figure for eGFR<60). A decline in eGFR was consistently associated with higher subsequent mortality risk (adjusted HR for -30% vs. 0% change in eGFR were: 1.8 at eGFR <60; and 1.6 at eGFR ≥60; p<0.001). Similar results were obtained for a 1- or 3-year change in eGFR. Hazards ratios were largely similar for those with eGFR ≥60 or when stratified by ACR levels. Conclusions: Declines in eGFR are strongly and consistently associated with subsequent risk of mortality adjusted for the first eGFR and covariates. These findings support using smaller changes than -57% (equivalent to doubling of serum creatinine) in clinical research

DECLINE IN ESTIMATED GLOMERULAR FILTRATION RATE AND SUBSEQUENT RISK OF MORTALITY: A META-ANALYSIS OF 35 COHORTS IN THE CKD PROGNOSIS CONSORTIUM

Introduction and Aims: Change in estimated GFR (eGFR) is frequently used to track CKD progression in clinical practice, trials and cohort studies but its association with mortality has not been studied extensively. Methods: Change in eGFR was estimated as % change from the first to last eGFR (CKD-EPI creatinine) in a 2-year baseline period.We modeled the hazard ratios (HRs) of subsequent mortality as a spline function of % change in eGFR after adjusting for age, sex, race, first eGFR, and co-morbid conditions.We used random effects meta-analyses to combine results stratified by first baseline eGFR (<60 & ≥60) across studies. Results: Mortality follow-up of 1,597,723 participants from 32 cohorts for a mean of 3.7 years after the 2-year baseline period showed 101,120 deaths for baseline eGFR <60 (n=395,394) and 57,472 deaths for baseline eGFR ≥60 (n=1,202,329). Change in eGFR had a non-linear association with mortality (Figure for eGFR<60). A decline in eGFR was consistently associated with higher subsequent mortality risk (adjusted HR for -30% vs. 0% change in eGFR were: 1.8 at eGFR <60; and 1.6 at eGFR ≥60; p<0.001). Similar results were obtained for a 1- or 3-year change in eGFR. Hazards ratios were largely similar for those with eGFR ≥60 or when stratified by ACR levels. Conclusions: Declines in eGFR are strongly and consistently associated with subsequent risk of mortality adjusted for the first eGFR and covariates. These findings support using smaller changes than -57% (equivalent to doubling of serum creatinine) in clinical research