scholarly journals Impact of Abdominal Aortic Calcification on Central Haemodynamics and Decline of Glomerular Filtration Rate in Patients with Chronic Kidney Disease Stages 3 and 4

2019 ◽  
Vol 44 (5) ◽  
pp. 950-960 ◽  
Author(s):  
Hanna Jansson ◽  
Aso Saeed ◽  
Maria K. Svensson ◽  
Kristina Finnved ◽  
Mikael Hellström ◽  
...  

Background/Aim: Calcifications of large arteries are frequent in chronic kidney disease (CKD) and may contribute to the high cardiovascular risk in this population. The aim of this study was to examine whether abdominal aortic calcification volume (AACV) was a predictor of the rate of decline in glomerular filtration rate (GFR) in a cohort of patients with CKD stages 3 and 4. Methods: Eighty-four patients with CKD stages 3 and 4 were enrolled in this prospective observational study. At study entry, and annually, GFR was measured by plasma 51Cr-EDTA clearance. At baseline, haemodynamics was assessed and AACV was determined by computer tomography. Results: The mean follow-up time was 3.4 years and mean decline in GFR was –2.69 mL/min/1.73 m2 per year. At baseline, abdominal aortic calcification (AAC) was detected in 66 patients (79%). A binary logistic regression analysis revealed that age was the only statistically significant independent predictor of AAC. In patients with AAC, male gender (B = 0.413, p = 0.030), aortic diastolic blood pressure (B = –0.025, p = 0.001) and ankle-brachial index (B = –1.666, p = 0.002) were independently associated with AACV using a multiple linear regression analysis. Neither the presence nor the extent of AAC was significantly associated with the rate of change in GFR during follow-up. Conclusion: In this cohort of patients with CKD stages 3 and 4, only age was an independent predictor of the presence of AAC. AACV was not associated with the rate of decline in GFR.

2021 ◽  
Vol 104 (6) ◽  
pp. 989-997

Background: Vascular calcification in advanced chronic kidney disease (CKD) is correlated with uremic toxins and severely impaired calciumphosphate- parathyroid metabolism. The association factors of vascular calcification in early-stage CKD are still unestablished. Objective: To identify the risk factors for vascular calcification in the early-stage CKD, which was the non-target population, different from other previous studies that explored this association in advanced stage CKD. Materials and Methods: The present study was a longitudinal study conducted to examine the risk factors of vascular calcification in CKD stage G2 and G3 patients who had no previous cardiovascular diseases. All parameters including coronary artery calcification (CAC) and abdominal aortic calcification (AAC) at baseline and after twelve months were evaluated. Results: Twenty-two patients without established cardiovascular diseases were included and completed the follow-up period. Mean baseline LDL was 99 mg/dL and no patient received statin. At 12-month, the median CAC score was significantly increased to 266 (126 to 956) versus 282 (198 to 846), (p=0.024]. By multivariable analysis in generalized estimating equations, only estimated glomerular filtration rate (eGFR) was associated with CAC score greater than 400 (aOR 0.92, p=0.041), and AAC score greater than 5 (aOR 0.90, p=0.023). Conclusion: In early-stage CKD, eGFR was associated with vascular calcification. Further studies should explore the potential benefits of delaying CKD progression on vascular calcification in the early-stage CKD patients. Keywords: Chronic kidney disease; Vascular calcification; Coronary artery calcification; Abdominal aortic calcification; Glomerular filtration rate; Renal function


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
SO MI KIM ◽  
Jong Tae Cho ◽  
Ji Hyun Jeon ◽  
Yong-Moon Lee ◽  
Eun Kyoung Lee ◽  
...  

Abstract Background and Aims Although abdominal aortic calcification (AAC) is known to be associated with cardiovascular mortality in patients with chronic kidney disease (CKD), there are little information about the impact of AAC on progression of CKD. Therefore, we investigated the relationship between the AAC and progression of renal insufficiency in CKD patients with early stage. Method A total of 183 patients with CKD, stage 3 was included. The degree of AAC was evaluated by computed tomography and the score was calculated as follows: abdominal calcification index (ACI)= (total score of calcification on all slices)/12 × 1/(number of slices) × 100%. Based on tertile of ACI, the patients were divided into three groups: low-, intermediate-, and high-groups. The annual decline of glomerular filtration rate (GFR) and time to dialysis were assessed. Results The AAC was found (ACI > 0) in 129 patients (70.4%), and the mean ACI was 21.3 %. The average duration of follow-up was 46.9 months. The high ACI group showed higher annual decline in GFR compared to other groups (27.8 vs 14.5 vs 11.3 mL/min, p=0.042). During the follow-up, 68.8% (42/61) of high ACI group received dialysis and the time to dialysis was significantly shorter than other groups (14.8 vs. 25.8 vs.29.1 months, p=0.038) Conclusion In this study, we showed the AAC was associated with rapid progression of CKD. Evaluation of the AAC in CKD with early stage provides useful information for predicting the progression of CKD.


2020 ◽  
Vol 51 (9) ◽  
pp. 726-735
Author(s):  
Roosa Lankinen ◽  
Markus Hakamäki ◽  
Kaj Metsärinne ◽  
Niina S. Koivuviita ◽  
Jussi P. Pärkkä ◽  
...  

Background: Patients with advanced chronic kidney disease (CKD stage 4-5) have an increased risk of death. To study the determinants of all-cause mortality, we recruited 210 consecutive CKD stage 4-5 patients not on dialysis to the prospective Chronic Arterial Disease, quality of life and mortality in chronic KIDney injury (CADKID) study. Methods: One hundred seventy-four patients underwent maximal bicycle ergometry stress testing and lateral lumbar radiography to study abdominal aortic calcification score and echocardiography. Carotid and femoral artery intima-media thickness and elasticity and brachial artery flow-mediated dilatation were measured in 156 patients. Results: The duration of follow-up was 42 ± 17 months (range 134–2,217 days). The mean age was 61 ± 14 years, and the estimated glomerular filtration rate was 12 (11–15) mL/min/1.73 m2. Thirty-six (21%) patients died during follow-up (time to death 835 ± 372 days). Seventy-five and 21 patients had diabetes and coronary artery disease, respectively, and all but one had hypertension. In the respective multivariate proportional hazards models adjusted for age, sex, and coronary artery disease, the significant determinants of mortality were troponin T, N-terminal pro-B-type natriuretic peptide, maximal ergometry performance, abdominal aortic calcification score, E/e′ ratio, and albumin. Conclusion: Stress ergometry performance, abdominal aortic calcification score, E/e′ of echocardiography, and plasma cardiac biomarkers and albumin predict mortality in advanced CKD.


2015 ◽  
Vol 41 (1) ◽  
pp. 28-36 ◽  
Author(s):  
Li Yao ◽  
Yi-ting Sun ◽  
Wei Sun ◽  
Tian-hua Xu ◽  
Chuang Ren ◽  
...  

Aims: Vascular calcification is a risk factor for causing cardiovascular events and has a high prevalence among chronic kidney disease (CKD) patients. However, the molecular mechanism underlying this pathogenic process is still obscure. Methods: Vascular smooth muscle cells (VSMCs) were induced by a concentration of phosphorus (Pi) of 2.5 mM, and were subjected to cell calcification analyses. The effect of high Pi on the Wnt/β-catenin pathway was measured using a TOP/FOP-Flash reporter assay. The transcriptional regulation of β-catenin on PIT1 (a type III sodium-dependent phosphate cotransporter) was confirmed by promoter reporter and chromatin immunoprecipitation assays. The 5/6 nephrectomized rat was used as an in vivo model and was fed a high Pi diet to induce aortic calcification. Serum levels of phosphate, calcium, creatine, and blood urea nitrogen were measured, and abdominal aortic calcification was examined. Results: High Pi induced VSMC calcification, downregulated expression levels of VSMC markers, and upregulated levels of osteogenic markers. High Pi activated the Wnt/β-catenin pathway and β-catenin activity. β-Catenin was involved in the process of high Pi-induced VSMC calcification. Further investigation revealed that β-catenin transcriptionally regulated Pit1, a necessary player in VSMC osteogenic phenotype change and calcification. The in vivo study showed that β-catenin was involved in rat abdominal aortic calcification induced by high Pi. When knockdown expression of β-catenin in the rat model was investigated, we found that aortic calcification was reduced. Conclusion: These results suggest that β-catenin is an important player in high phosphorus level-induced aortic calcification in CKD.


2012 ◽  
Vol 17 (3) ◽  
pp. 365-371 ◽  
Author(s):  
Shunsuke Goto ◽  
Ken Kitamura ◽  
Keiji Kono ◽  
Kentaro Nakai ◽  
Hideki Fujii ◽  
...  

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257305
Author(s):  
Hyo Jin Kim ◽  
Tae Eun Kim ◽  
Miyeun Han ◽  
Yongin Yi ◽  
Jong Cheol Jeong ◽  
...  

Background Anemia is a common complication of chronic kidney disease (CKD). Blood urea nitrogen (BUN) in CKD represents nitrogenous uremic toxin accumulation which could be involved in anemia of CKD. We investigated the effects of BUN independent of estimated glomerular filtration rate (eGFR) on anemia in non-dialysis CKD (NDCKD). Methods This prospective study included 2,196 subjects enrolled in the KoreaN Cohort Study for Outcome in Patients With Chronic Kidney Disease (KNOW-CKD) cohort with BUN and hemoglobin level data. Initially, we investigated the association between BUN and hemoglobin level. To examine the impact of baseline BUN on the incident anemia, a longitudinal study was performed on 1,169 patients without anemia at study enrollment. BUN residuals were obtained from the fitted curve between BUN and eGFR. Anemia was defined as a hemoglobin level of <13.0 g/dL for men and <12.0 g/dL for women. Results BUN residuals were not related to eGFR but to daily protein intake (DPI), while BUN was related to both eGFR and DPI. BUN was inversely associated with hemoglobin level (β -0.03; 95% confidence interval [CI] -0.04, -0.03; P <0.001) in the multivariable linear regression analysis adjusted for multiple confounders including eGFR, and BUN residual used instead of BUN was also inversely associated with hemoglobin level (β -0.03; 95% CI -0.04, -0.02; P <0.001). Among the 1,169 subjects without anemia at baseline, 414 (35.4%) subjects newly developed anemia during the follow-up period of 37.5 ± 22.1 months. In the multivariable Cox regression analysis with adjustment, both high BUN level (Hazard ratio [HR] 1.02; 95% CI 1.01, 1.04; P = 0.002) and BUN residual used instead of BUN (HR 1.02; 95% CI 1.00, 1.04; P = 0.031) increased the risk of anemia development. Moreover, BUN, rather than eGFR, increased the risk of anemia development in patients with CKD stage 3 in the multivariable Cox regression. Conclusion Higher BUN levels derived from inappropriately high protein intake relative to renal function were associated with low hemoglobin levels and the increased risk of anemia independent of eGFR in NDCKD patients.


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