Cardiac remodelling and functional alterations in mild‐to‐moderate renal dysfunction: comparison with healthy subjects

Anna, Moiseeva; Wallquist, Carin; Rickenlund, Anette; Hylander, Britta; Jacobson, Stefan H.; Caidahl, Kenneth; Eriksson, Maria

doi:10.1111/cpf.12154

Cited by 23 publications

(26 citation statements)

References 38 publications

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“…The methodological details have been described previously (Jensen-Urstad & Rosfors, 1997;Asp et al, 2015;Asp et al, 2018). The methodological details have been described previously (Jensen-Urstad & Rosfors, 1997;Asp et al, 2015;Asp et al, 2018).…”

Section: Ultrasound Examinationsmentioning

confidence: 99%

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Cardiovascular changes in patients with mild‐to‐moderate chronic kidney disease compared with healthy subjects: a 5‐year follow‐up study

Anna¹,

Wallquist²,

Rickenlund³

et al. 2019

Clin Physio Funct Imaging

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Background There is limited knowledge about how cardiovascular parameters change over time in patients with mild-to-moderate chronic kidney disease (CKD). We studied several cardiovascular biomarkers over a 5-year period in patients with mild-to-moderate CKD and in healthy controls. Methods Fifty-four patients with CKD stages 2-3 and 54 controls were included. The CKD patients were closely monitored and well controlled for hypertension and other cardiovascular risk factors. Ambulatory blood pressure (BP) monitoring, ankle-brachial index (ABI), carotid and cardiac ultrasound (including measurement of the left ventricular mass index (LVMI)), and biochemical analyses were evaluated. Results Renal function decreased in both groups, with no significant difference in the change over time. In the CKD patients, none of the BP variables increased over time, but in the controls, average 24-h and daytime systolic BP increased significantly. ABI increased slightly in the CKD patients (P<0Á001), but not in the controls (P = 0Á963), and phosphate had a significant positive effect on ABI. Although in the CKD patients, there was no significant increase over time in common carotid artery diameter (P = 0Á274), there was a small but significant increase in the controls (P = 0Á001). LVMI increased significantly over time in both groups. Conclusions In our study of patients with mild-to-moderate CKD, the progression of cardiovascular changes over time was relatively slow. Good BP control and treatment of other risk factors may have contributed to slow the progress of cardiovascular involvement, which emphasizes the importance of dedicated care in this population.

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Section: Ultrasound Examinationsmentioning

confidence: 99%

“…The ultrasound examinations were performed by two experienced sonographers, using an ultrasound machine (Sequoia 512; Siemens Medical Solutions, Mountain View, CA, USA) with an appropriate transducer. The methodological details have been described previously (Jensen-Urstad & Rosfors, 1997;Asp et al, 2015;Asp et al, 2018).…”

Section: Ultrasound Examinationsmentioning

confidence: 99%

Cardiovascular changes in patients with mild‐to‐moderate chronic kidney disease compared with healthy subjects: a 5‐year follow‐up study

Anna¹,

Wallquist²,

Rickenlund³

et al. 2019

Clin Physio Funct Imaging

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“…The patients and healthy controls were included in a prospective single-centre observational cohort study, PROGRESS 2002, which was described in detail previously (Asp et al, 2015). Briefly, 103 Swedish-speaking CKD patients not on dialysis, 18-65 years of age, and 54 controls were included.…”

Section: Patients and Control Subjectsmentioning

confidence: 99%

Aspects of carotid structure and function in health and different stages of chronic kidney disease

Anna

Wallquist

Rickenlund

et al. 2017

Clin Physio Funct Imaging

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Introduction Arterial remodelling and stiffening have been demonstrated in endstage renal disease (ESRD). The presence of vascular alterations in earlier-stage chronic kidney disease (CKD) is less studied. We evaluated vascular structure and function in mild-to-moderate CKD (stages 2-3) compared with healthy subjects and advanced CKD (stages 4-5). Methods Carotid ultrasound was performed in 103 non-dialysis CKD patients and 54 healthy controls. Carotid intima-media thickness (CIMT) and common carotid artery (CCA) diameter were measured. Strain, stiffness and the pressure-strain elastic modulus (E p ) of the right CCA were calculated. Results There was no significant difference in CCA diameter between CKD 2-3 and controls. The CCA diameter was larger in CKD 4-5 compared with CKD 2-3 and controls (CKD 4-5, 6Á50 AE 0Á79 mm versus CKD 2-3, 6Á08 AE 0Á56 mm, P = 0Á003; and versus controls 5Á97 AE 0Á53 mm, P<0Á001). However, after adjustments, the difference in CCA diameter was valid only for older ages and also dependent on systolic blood pressure (SBP). There were no significant differences in CIMT, strain or stiffness between the groups, but E p was higher in CKD 4-5 compared with controls (P = 0Á006). Conclusion In mild-to-moderate CKD, there were no significant differences in carotid artery structure or function compared with healthy subjects. Only patients with advanced CKD and older ages showed signs of arterial remodelling. Our study indicates that vascular alterations occur in advanced CKD, with SBP and age as important contributing factors.

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“…The PROGRESS cohort, previously described in detail [24], was applied for this study. Briefly, 103 patients aged 18-62 years with mild to moderate or severe CKD were recruited.…”

Section: Study Populationmentioning

confidence: 99%

Associations of Fibroblast Growth Factor 23 with Markers of Inflammation and Leukocyte Transmigration in Chronic Kidney Disease

Wallquist

Mansouri

Norrbäck

et al. 2018

Nephron

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Background: Patients with chronic kidney disease (CKD) show elevated levels of inflammatory markers and have an increased risk of infections as well as cardiovascular morbidity. Recent studies have implied effects of fibroblast growth factor 23 (FGF23) on inflammation in CKD. We analyzed potential correlations between levels of FGF23 with pro-inflammatory chemokines and markers of leukocyte transmigration in CKD patients. Methods: One hundred three patients with CKD 2–5ND and 54 healthy controls, had biochemical markers in blood and urine analyzed according to routine protocol. Pro-inflammatory cytokines were analyzed by Milliplex technique and leukocyte CD11b adhesion molecule expression was measured by flow cytometry. FGF23 levels were measured with ELISA technique. Treatment of leukocytes from healthy blood donors with FGF23 was performed in vitro and effects analyzed by flow cytometry. Results: Tumor necrosis factor-alpha, RANTES and interleukin (IL)-12 levels were significantly higher (p = 0.001, p < 0.001, and p < 0.001) in patients with CKD. Elevated FGF23 levels in the CKD group correlated to glomerular filtration rate, parathyroid hormone, urinary albumin excretion and phosphate as well as to IL-12 and RANTES. CD11b expression on resting granulocytes and monocytes, and on activated monocytes, was associated with FGF23. In vitro treatment of leukocytes with FGF23 reduced CD11b expression in resting as well as in formyl-methyinoyl-leucyl-phenylalanine-stimulated granulocytes (p = 0.03). Conclusion: FGF23 levels are associated with various inflammatory markers such as pro-inflammatory cytokines and adhesion molecules on innate immune cells. However, further studies are warranted to define the direct role of FGF23 in modulation of the innate immune system in CKD.

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Cardiac remodelling and functional alterations in mild‐to‐moderate renal dysfunction: comparison with healthy subjects

Cited by 23 publications

References 38 publications

Cardiovascular changes in patients with mild‐to‐moderate chronic kidney disease compared with healthy subjects: a 5‐year follow‐up study

Cardiovascular changes in patients with mild‐to‐moderate chronic kidney disease compared with healthy subjects: a 5‐year follow‐up study

Aspects of carotid structure and function in health and different stages of chronic kidney disease

Associations of Fibroblast Growth Factor 23 with Markers of Inflammation and Leukocyte Transmigration in Chronic Kidney Disease

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