BackgroundThe cause of reduced exercise capacity (ExCap) in chronic kidney disease (CKD) is multifactorial. The aim of this study was to investigate determinants of aerobic ExCap in patients with mild to severe CKD not undergoing dialysis.MethodsWe included 52 individuals with CKD stage 2–3, 47 with stage 4–5, and 54 healthy controls. Peak workload and peak heart rate (HR) were assessed by a maximal cycle exercise test. Cardiac function including stroke volume (SV) and vascular stiffness were evaluated by ultrasound at rest. Handgrip strength, body composition, haemoglobin level and self-reported physical activity were assessed.ResultsPeak workload (221±60, 185±59, 150±54 W for controls, CKD 2–3 and CKD 4–5 respectively), peak HR (177±11, 161±24, 144±31 beats/min) and haemoglobin level (14.2±1.2, 13.5±1.4, 12.2±1.3 g/dL) were all three significantly lower in CKD 2–3 than in controls, (p = 0.001, 0.001 and 0.03 respectively) and were even lower in stages 4–5 CKD than in CKD 2–3 (p = 0.01, 0.001 and <0.001 respectively). Resting SV and lean body mass did not differ between groups and handgrip strength was significantly lower only in CKD 4–5 compared to controls (p = 0.02). Peak workload was strongly associated with the systemic oxygen delivery factors: SV, peak HR and haemoglobin level. These three factors along with age, sex and height2 explained 82% of variation in peak workload. Peak HR contributed most to the variation; the peripheral variables handgrip strength and vascular stiffness did not improve the explanatory value in regression analysis.ConclusionsIn this cross-sectional study of CKD patients not on dialysis, aerobic ExCap decreased gradually with disease severity. ExCap was associated mainly with systemic oxygen delivery factors, in particular peak HR. Neither muscle function and mass, nor vascular stiffness were independent determinants of aerobic ExCap in this group of CKD patients.
IntroductionLeft ventricular (LV) hypertrophy (LVH) and reduced LV function correlate with poor prognosis in patients with chronic kidney disease (CKD). Our aim is to investigate whether mild-to-moderate CKD is associated with cardiac abnormalities.MethodsEchocardiography, including tissue Doppler imaging, was performed in 103 patients with CKD at stages 2–3 and 4–5, and in 53 healthy controls. The systolic (s′) and diastolic myocardial velocity (e′), and the transmitral diastolic flow velocity (E) were measured, and E/e′ was calculated.ResultsPatients with chronic kidney disease had higher mean E/e′ than controls (mean E/e′: controls 5·00 ± 1·23 versus CKD 4–5 6·36 ± 1·71, P<0·001 and versus CKD 2–3 5·69 ± 1·47, P = 0·05), indicating altered diastolic function in the patients. The CKD groups showed lower longitudinal systolic function than controls, as assessed by atrio-ventricular plane displacement and s′ (mean s′: controls 11·5 ± 1·9 cm s−1 versus CKD 4–5 10·4 ± 2·1 cm s−1, P = 0·03 and versus CKD 2–3 10·4 ± 2·1 cm s−1, P = 0·02). The prevalence of LVH was higher in patients with CKD than in controls (controls 13% versus CKD 4–5 37%, P = 0·006 and versus CKD 2–3 30%, P = 0·03).ConclusionAlterations in systolic and diastolic myocardial function can be seen in mild-to-moderate CKD compared with controls, indicating that cardiac involvement starts early in CKD, which may be a precursor of premature cardiac morbidity.
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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