Abstract 546: Arterial Stiffness And Pulse Pressure Predict Kidney Disease Progression In Chronic Kidney Disease

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Raymond Townsend ◽  
Nisha Bansal ◽  
Julio Chirinos ◽  
Magdalena Cuevas ◽  
Virginia Ford ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Arterial Stiffness ◽  
Disease Progression ◽  
Pulse Pressure ◽  
Cox Regression ◽  
Ckd Progression ◽  
Multivariable Regression ◽  
Kidney Disease Progression ◽  
Progression Prediction

Brachial pulse pressure (bPP) predicts kidney function in CKD. Pulse wave velocity (PWV) may provide additional prediction of CKD progression, and was evaluated longitudinally in CKD patients enrolled in the CRIC cohort. bPP was used because it shows superior CKD progression prediction in humans. There were 2821 participants in CRIC who underwent an assessment of PWV most of whom were studied at their second year follow-up visit. Of these 43 % were women, 48% diabetic, mean age 60 years and mean estimated GFR of 44.6 mL/min/1.73m2. Blacks were 40%, whites 44%, and Hispanics 12%. Mean blood pressure was 127/70 mmHg; mean bPP was 54 mmHg. The interaction of PWV with bPP on the occurrence of ESRD (dialysis or a transplant) [left panel of figure] and a combined endpoint of halving of the eGFR or ESRD [right panel], was analyzed used Cox regression. Events by tertiles of PWV (<7.9 msec; 7.9-10.3 m/sec; >10.3m/sec) and bPP (<46 mmHg, 46-62 mmHg, >62 mmHg) are shown in the figure. There were significant interactions between PWV and bPP for both outcomes. For ESRD the hazard ratio of the highest tertiles of PWV/bPP compared with the lowest was 3.18 (p<0.001). For the combined ESRD or halving of eGFR the HR was 2.65 (p<0.001). In multivariable regression important predictors of CKD progression in this model were age, male gender, non-white race/ethnicity, initial eGFR, and proteinuria.PWV showed a strong and graded interaction with bPP in the prediction of ESRD and the combined outcome of halving of GFR or ESRD. A greater appreciation of the role of arterial stiffness in CKD is an important step towards pursuing the mechanisms underlying how this measure may influence the course of kidney disease progression.

scholarly journals P0741CHRONIC KIDNEY DISEASE PROGRESSION IN A LARGE PREVENTION COHORT IN COLOMBIA

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Angela Rivera ◽  
Angelito Bernardo ◽  
Jasmin Vesga ◽  
Izcay Ronderos ◽  
Mauricio Sanabria
Keyword(s):  
Kidney Disease ◽  
Disease Progression ◽  
Prevention Program ◽  
Reduction Rate ◽  
Progression Rate ◽  
Ckd Progression ◽  
Care Services ◽  
Kaplan Meier ◽  
Observational Cohort ◽  
Kidney Disease Progression

Abstract Background and Aims Chronic kidney disease (CKD) is a syndrome that today has important implications for the health of populations and the economic sustainability of health systems around the world, therefore strategies to slow disease progression are necessary. Aims: To estimate the incidence of renal replacement therapy (RRT) in a cohort of patients included in a CKD secondary prevention program and to describe the decrease of the estimated glomerular filtration rate (eGFR). Method This is a historical, multicenter, observational cohort study in a prevention program between January 1, 2010, and December 31, 2017, with follow-up until December 31, 2018, at the Renal Care Services (RCS) network. Socio-demographic and clinical characteristics of all patients were summarized descriptively. We estimated the incidence of RRT rate with Kaplan Meier analysis. Progression rate to RRT was analyzed by mixed-effects model adjusted for the eGFR reduction rate at 180 days; the model considered the diagnosis of diabetes. Results 7131 patients met the inclusion criteria for data analysis. The mean age was 65 years, 50.5% were female, (Table 1). There were 577 events of RRT with a rate of 2.02 events of RRT per 100 patients-year [95% CI,1.86 to 2.19], characteristics at the RRT initiation are presented in Table 2. At the beginning of the program the eGFR was 45.3 ml / min / 1.73m2 in non-diabetics, and 40.9 3 ml / min / 1.73m2 in diabetics. The CKD progression was - 0.48 ml / min / 1.73m2 per 180 days in diabetics and - 0.20 ml / min / 1.73m2 per 180 days in non-diabetics. The final events of the cohort are presented in Figure 1; the mortality rate was 0.89 events per 100 patients-year [95% CI, 0,79 to 1,01]. Conclusion This population of patients in a CKD prevention program presented a low rate of initiation of dialysis therapy and a slight decrease of eGFR; the diabetic status influences the CKD progression.

scholarly journals Obesity and chronic kidney disease progression—the role of a new adipocytokine: C1q/tumour necrosis factor-related protein-1

2018 ◽  
Vol 12 (3) ◽  
pp. 420-426 ◽  
Author(s):  
Diego Barbieri ◽  
Marian Goicoechea ◽  
Maria Dolores Sánchez-Niño ◽  
Alberto Ortiz ◽  
Eduardo Verde ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Disease Progression ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Related Protein ◽  
Chronic Kidney Disease Progression ◽  
Kidney Disease Progression ◽  
Necrosis Factor

scholarly journals Arterial stiffness and kidney disease progression in the systolic blood pressure intervention trial

2020 ◽  
Vol 94 (1) ◽  
pp. 26-35
Author(s):  
Kristen L. Nowak ◽  
Michel Chonchol ◽  
Anna Jovanovich ◽  
Zhiying You ◽  
Walter T. Ambrosius ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Systolic Blood Pressure ◽  
Disease Progression ◽  
Intervention Trial ◽  
Kidney Disease Progression

MO250URINARY DICKKOPF-3 (UDKK3): A NEW BIOMARKER FOR LONG-TERM CKD PROGRESSION AND MORTALITY?*

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Beatriz Sanchez Alamo ◽  
Francisco Jose Garcia Iñigo ◽  
Amir Shabaka ◽  
Juan Manuel Acedo ◽  
Clara Maria Cases Corona ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Renal Fibrosis ◽  
Primary Outcome ◽  
Creatinine Ratio ◽  
Ckd Progression ◽  
Kidney Disease Progression ◽  
Renal Progression

Abstract Background and Aims Kidney fibrosis has been reported to be a key progression hallmark of chronic kidney disease (CKD). It seems likely that a precise biomarker of renal fibrosis extension would contribute to predict accurately the risk of a decline in glomerular filtration rate (eGFR). Previous studies have shown that the assessment of urinary Dickkopf-3 (uDKK3), a stress induced tubular epithelial-derived profibrotic glycoprotein, might be a potential tubulointerstitial fibrosis biomarker and might identify patients at short-term risk of eGFR loss. We aim to evaluate uDKK3 as a potential biomarker for long-term CKD progression in a cohort with various etiologies of CKD, and subsequently in an overt diabetic nephropathy cohort. We also tested the role of treatment with RAAS blockers on the uDKK3 levels and if the treatment could modify them. Method We prospectively studied two independent cohorts consisted of 356 patients with stage 2-3 CKD. Progreser cohort comprised 255 patients with heterogeneous etiologies of CKD and Pronedi cohort 101 patients with overt diabetic nephropathy. The primary outcome was the time to the first event of the composite endpoint (&gt;50% increase in serum creatinine concentration, end-stage kidney disease [ESKD], or death). We divided patients into tertiles according to their baseline uDKK3 levels: less than 1092 pg/mg (Tertile 1, T1), between 1092-5050 pg/mg (Tertile 2, T2) and higher than 5050 pg/mg (Tertile 3, T3). We used the cut point of T3 as an exploratory cut-off. Cox regression models were used to adjust for potential effects of confounders or modifiers: age, gender, mean arterial pressure, body mass index (BMI), urine albumin/creatinine ratio, urine protein/creatinine ratio and serum creatinine. Mixed-effects models were adjusted to study longitudinal data. Results Progreser cohort and Pronedi cohort did not differ in their clinical baseline characteristics except in proteinuria. At baseline, uDKK3 levels were not different between different etiologies or both cohorts, median uDKK3 was 2199 (IQR: 658-7618) pg/mg in the Progreser cohort and 3041 (IQR: 653-9777) pg/mg in the Pronedi cohort (p:0.56). Median time of follow-up was 36 months. Forty-nine patients (19 %) in Progreser cohort and 31 patients (31%) in Pronedi cohort reached the primary composite outcome. Baseline uDKK3 was significantly higher in patients who reached primary outcome. In Cox multivariate model, after adjustment for potential confounders, the highest levels of uDKK3 were found to be an independent factor for renal progression in Progreser cohort (HR 1.83, CI95% 1.11-3.31) and in Pronedi cohort (HR 2.74, CI95% 1.09-6.98). Both in the Progreser and the Pronedi cohorts, uDKK3 levels above 5050 pg/mg, were associated with a lower eGFR, higher proteinuria and were independently associated with a worse renal survival. uDKK3 gradually increased in the following months, especially in patients with higher proteinuria. Treatment with RAAS-blockers did not modify uDKK3 after 4 or 12 months of treatment. Conclusion In this study, uDKK3 ratio identified patients at high risk for long-term kidney disease progression regardless of the etiology of CKD. The hypothesis was generated in a cohort of patients with CKD of heterogeneous etiologies and was further confirmed in a cohort with overt diabetic nephropathy. The predictive role of uDKK3 persisted after adjusting by eGFR and proteinuria. uDKK3 is the first non-invasive biomarker of renal fibrosis and might serve as a useful biomarker for kidney disease progression. Therefore uDKK3 could be used by clinicians to optimize staging for renal progression and monitor therapeutic efficacy of different measures to halt CKD progression.

153: Pulse Pressure as a Predictor of Chronic Kidney Disease Progression

2008 ◽  
Vol 51 (4) ◽  
pp. B66
Author(s):  
A. Bilal Malik ◽  
Melissa Shannon ◽  
Lavanya Amuluru ◽  
Irfan Kundi ◽  
M. Gohar Alam
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Disease Progression ◽  
Pulse Pressure ◽  
Chronic Kidney Disease Progression ◽  
Kidney Disease Progression

Evidence for a role of uromodulin in chronic kidney disease progression

2010 ◽  
Vol 25 (6) ◽  
pp. 1896-1903 ◽  
Author(s):  
S. Prajczer ◽  
U. Heidenreich ◽  
W. Pfaller ◽  
P. Kotanko ◽  
K. Lhotta ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Disease Progression ◽  
Chronic Kidney Disease Progression ◽  
Kidney Disease Progression
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