The combination of chronic kidney disease and increased arterial stiffness is a predictor for stroke and cardiovascular disease in hypertensive patients

Abstract Background and Aims 24-h blood pressure (BP) may be superior to office BP in the prediction of cardiovascular mortality and also central aortic BP may better predict outcomes than brachial one. Hypertensive patients with type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) have higher risk and poorer BP control than patients with normal glycemic state and renal function. 24-h profile of central BP and arterial stiffness according to CKD phenotypes are not well described in this population. The aim of the study was to evaluate the associations of kidney function and proteinuria with 24-h central BP and parameters of arterial stiffness in hypertensive patients with T2DM and CKD. Method 90 patients with hypertension (HTN), T2DM and CKD (eGFR 30-60 ml/min/1.73 m2 and morning spot urine albumin–creatinine ratio (UACR) <300 mg/g) were included. 66% of them were females, median age was 60 years, 69% were smokers, 53% obese, 77% with dyslipidemia. Median duration of T2DM and HTN was 7.5 years and 18 years, respectively. All received antihypertensive drugs (77% – combinations of 2 or 3 drugs) and glucose lowering therapy (insulin in 58%). The analysis was performed according to CKD phenotype: proteinuric (UACR 30-300 mg/g) and non-proteinuric (UACR <30 mg/g) and according to CKD stage assessed by GFR (G3a and G3b, KDIGO (2012)). Office brachial BP was measured with a validated oscillometric device. Office aortic BP and arterial stiffness were assessed with applanation tonometry (SphygmoCor AtCor). 24-hour ABPM of brachial and aortic BP was performed with BPLab Vasotens. All results are presented as median values. P<0.05 was considered significant. Results Median brachial BP was 156/83 mmHg, aortic BP 139/90 mmHg. Median eGFR was 53 ml/min/1.73 m2, UACR – 62.2 mg/g. Phenotypes of CKD were as follows: proteinuric in 78% (GFR 50 ml/min/1.73 m2, UACR 62 mg/g) and non-proteinuric in 22 % (GFR 54 ml/min/1.73 m2, med UACR 5 mg/g, p<0.01 for trend compared non-proteinuric). Patients with proteinuric phenotype compared to non-proteinuric were characterized by higher rate of dyslipidemia (85% vs 45%, p<0.001), longer duration of HTN and DM (19.5 vs 7.5 years and 8 vs 3 years, respectively, p <0.01 for trend) and lower HDL-C (1.2 vs 1.9, p=0.02). Both groups had similar office brachial SBP (156 vs 157 mmHg; p=0.48), but patients with proteinuric phenotype had higher office central SBP (147 vs 137 mmHg, p=0.007) and worse 24-h profile of central SBP (daytime 147 vs 138 mmHg, p=0.008; night-time 143 vs 130 mmHg, p=0.04). Proteinuric phenotype significantly correlated with office aortic SBP (r=0.28; p=0.01) and daytime and night-time aortic SBP (r=0.28 and 0.21 respectively, p <0.05 for trend). The eGFR phenotypes were as follows: G3a in 82.2% (GFR 54 ml/min/1.73 m2, UACR 20 mg/g) and G3b in 17.8% (GFR 38 ml/min/1.73 m2, med UACR 46 mg/g, p<0.01 for trend compared to G3a). Patients with worse kidney function had longer duration of HTN and DM (16 vs 11 years and 10 vs 6 years, respectively, p <0.01 for trend), higher median brachial and aortic BP levels (158/90 vs 146/82 mmHg and 150/95 vs 138/80 mmHg, respectively, p<0.01 for trend), worse 24-h profile of central SBP (daytime 148 vs 138 mmHg, p=0.008; night-time 146 vs 130 mmHg, p=0.006), higher central pulse pressure (56 vs 49 mmHg, p=0.007), augmentation index (33 vs 14%, p=0.007). Conclusion Hypertensive patients with T2DM and CKD G3b and proteinuria were characterized by worse 24-profile of central BP and higher arterial stiffness.

Download Full-text

Renal bone disease: a dietitian's perspective

Journal of Kidney Care ◽

10.12968/jokc.2020.5.1.18 ◽

2020 ◽

Vol 5 (1) ◽

pp. 18-25

Author(s):

Ruth Kander

Keyword(s):

Cardiovascular Disease ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Arterial Stiffness ◽

Dietary Restriction ◽

Bone Disease ◽

Morbidity And Mortality ◽

Phosphate Binders ◽

Renal Bone Disease ◽

High Phosphate

Renal bone disease increases morbidity and mortality in patients with chronic kidney disease by increasing the risk for fractures, osteoporosis and other bone problems and its association with cardiovascular disease, including calcification and arterial stiffness. Treatment of renal bone disease is through a combination of three main methods to reduce phosphate levels: dietary restriction of high-phosphate foods; dialysis clearance; and the use of phosphate binders to prevent its absorption.

Download Full-text

Nontraditional Biomarkers for Cardiovascular Disease in Patients With Chronic Kidney Disease

Ramathibodi Medical Journal ◽

10.33165/rmj.2020.43.2.230208 ◽

2020 ◽

Vol 43 (2) ◽

pp. 51-60

Author(s):

Ittikorn Spanuchart ◽

Arkom Nongnuch ◽

Youg Liu

Keyword(s):

Cardiovascular Disease ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Arterial Stiffness ◽

Mineral Metabolism ◽

Uremic Toxins ◽

Calcium Balance ◽

The Novel ◽

Cvd Risk ◽

Chd Risk

Cardiovascular disease (CVD) is the leading cause of death among patients who have chronic kidney disease (CKD). Nowadays, CKD per se is considered one of the coronary heart disease (CHD) risk equivalents. Apart from traditional CVD risk factors, there are several possible determinants for CVD in patients with CKD, for example, uremic toxins, increased inflammatory stage, abnormal bone mineral metabolism, and positive calcium balance. In this narrative review, we offer a summary of the extensively studied biomarkers for CVD in patients with CKD, including uremic toxins (p-cresol, indoxyl sulfate, and advanced glycated end products), and a novel indicator of arterial stiffness, cardio-ankle vascular index (CAVI), which is an independent prognostic predictor for CVD. For the uremic toxins, we reviewed their metabolisms, particularly, how the reduced renal function in CKD patients affect their clearance and their clearance with dialysis. Also, we pay attention to the recent evidence on how those uremic toxins contribute to CVD and their clinical associations. We do not include the possible treatment targeting at those uremic toxins. As for the novel indicator of arterial stiffness, we reviewed the clinical application of CAVI in comparison to the standard indicator for arterial stiffness, pulse wave velocity.

Download Full-text

Ambulatory Arterial Stiffness Index Is Higher in Hypertensive Patients with Chronic Kidney Disease

International Journal of Hypertension ◽

10.1155/2012/178078 ◽

2012 ◽

Vol 2012 ◽

pp. 1-6 ◽

Cited By ~ 7

Author(s):

Ronaldo Altenburg Gismondi ◽

Mario Fritsch Neves ◽

Wille Oigman ◽

Rachel Bregman

Keyword(s):

Blood Pressure ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Arterial Stiffness ◽

Blood Pressure Monitoring ◽

Stiffness Index ◽

Hypertensive Patients ◽

Clinical Endpoints ◽

Mdrd Formula ◽

Arterial Stiffness Index

Ambulatory arterial stiffness index (AASI) is a parameter obtained from ambulatory blood pressure monitoring (ABPM) that correlates with clinical endpoints. The aim of this study was to compare AASI in nondiabetic hypertensive patients with and without chronic kidney disease (CKD). Subjects with systemic arterial hypertension (SAH,n=30) with normal renal function, aged 40 to 75 years, were compared to hypertensive patients with CKD (n=30) presenting estimated glomerular filtration rate (eGFR) <60 mL/min by MDRD formula. ABPM was carried out in all patients. In CKD group, eGFR was 35.3 ± 2.8 ml/min. The mean 24-hour systolic and diastolic blood pressure (BP) was similar in both groups. AASI was significantly higher in CKD group (0.45±0.03versus0.37±0.02,P<0.05), positively correlated to age (r=0.38,P<0.01) and pulse pressure (r=0.43,P<0.01) and negatively correlated to nocturnal BP fall (r=-0.28,P=0.03). These findings indicate the presence of stiffer vessels in CKD hypertensive patients.

Download Full-text

Cardiovascular Disease Risk in Children With Chronic Kidney Disease: Impact of Apolipoprotein C-II and Apolipoprotein C-III

Frontiers in Pediatrics ◽

10.3389/fped.2021.706323 ◽

2021 ◽

Vol 9 ◽

Author(s):

Wei-Ling Chen ◽

You-Lin Tain ◽

Hung-En Chen ◽

Chien-Ning Hsu

Keyword(s):

Cardiovascular Disease ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Arterial Stiffness ◽

Left Ventricular ◽

Differentially Expressed ◽

Surrogate Markers ◽

Differentially Expressed Proteins ◽

Apolipoprotein C ◽

Lv Mass

Cardiovascular disease (CVD) is an evolving process that begins in the early stages of chronic kidney disease (CKD) in children. Several surrogate markers, such as ambulatory blood pressure monitoring (ABPM), left ventricular (LV) mass, and arterial stiffness assessment, allow for the early detection of subclinical CVD in pediatric CKD. Four groups of plasma samples (n = 3/group) from congenital anomalies of the kidney and urinary tract (CAKUT), as well as non-CAKUT patients with or without BP abnormalities, were studied to screen differentially expressed proteins using isobaric tags for relative and absolute protein quantification (iTRAQ)-based proteomics. As a result, 20 differentially expressed proteins associated with hypertension in children with CKD were discovered. Among them, apolipoprotein C-II (apoC-II) was found to have the highest abundance among the CKD patients with hypertension. As such, we hypothesized that apoC-II and apolipoprotein C-III (apoC-III) levels were related to BP abnormalities and CVD in children suffering from mild-to-moderate CKD. We examined their associations with surrogate markers of CV risk in 88 pediatric patients with CKD stages G1–G4. Children with CKD stages G2–G4 had a higher plasma apoC-II level than G1 patients (6.35 vs. 5.05 mg/dl, p < 0.05). We observed that ABPM abnormalities, LV mass, and arterial stiffness parameters were greater in CKD children who had stages G2–G4 than in those who had stage G1 (all p < 0.05). Plasma levels of apoC-II and apoC-III were positively correlated with total cholesterol, triglyceride, and low-density lipoprotein (LDL) (all p < 0.001). In multivariate linear regression analyses, apoC-II was correlated with a high LV mass index and an abnormal ABPM profile, and apoC-III was correlated with 24-h hypertension (r = 0.303, p = 0.003) and asleep hypertension (r = 0.379, p < 0.001). Early evaluations of apoC-II and apoC-III, ABPM, and surrogate markers of CV risk will aid in early preventative interventions to reduce the risk of CV in youths suffering from CKD.

Download Full-text

Effects of oral paricalcitol therapy on arterial stiffness and osteopontin in hypertensive patients with chronic kidney disease and secondary hyperparathyroidism

Hellenic Journal of Cardiology ◽

10.1016/j.hjc.2017.12.010 ◽

2019 ◽

Vol 60 (2) ◽

pp. 108-113 ◽

Cited By ~ 4

Author(s):

Michalis Giakoumis ◽

Costas Tsioufis ◽

Kyriakos Dimitriadis ◽

Makro Sonikian ◽

Alexandros Kasiakogias ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Arterial Stiffness ◽

Secondary Hyperparathyroidism ◽

Hypertensive Patients

Download Full-text

[PP.07.05] ORAL PARICALCITOL THERAPY REDUCES ARTERIAL STIFFNESS IN HYPERTENSIVE PATIENTS WITH CHRONIC KIDNEY DISEASE AND SECONDARY HYPERPARATHYROIDISM

Journal of Hypertension ◽

10.1097/01.hjh.0000523363.77422.03 ◽

2017 ◽

Vol 35 ◽

pp. e138

Author(s):

K. Dimitriadis ◽

K. Tsioufis ◽

M. Giakoumis ◽

Th. Kalos ◽

M. Kouremeti ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Arterial Stiffness ◽

Secondary Hyperparathyroidism ◽

Hypertensive Patients

Download Full-text

Changes in FGF-23, Neutrophil/Platelet Activation Markers, and Angiogenin in Advanced Chronic Kidney Disease and Their Effect on Arterial Stiffness

Kidney & Blood Pressure Research ◽

10.1159/000502526 ◽

2019 ◽

Vol 44 (5) ◽

pp. 1166-1178

Author(s):

Hye-Min Choi ◽

Young-Eun Kwon ◽

Sol Kim ◽

Dong-Jin Oh

Keyword(s):

Cardiovascular Disease ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Arterial Stiffness ◽

Platelet Activation ◽

Activation Markers ◽

Stage 4 ◽

Ckd Stage ◽

The Mean ◽

Fgf 23

Aims: The aims of this study were to measure changes in fibroblast growth factor 23 (FGF-23), neutrophil (elastase, lactoferrin)/platelet activation marker (mean platelet volume-to-platelet count ratio [MPR]), and angiogenin according to the stage of chronic kidney disease (CKD), and to evaluate the association of FGF-23, elastase, lactoferrin, MPR, and angiogenin with arterial stiffness using brachial-ankle pulse wave velocity (ba-PWV) in CKD patients. Methods: According to the estimated glomerular filtration rate (eGFR) calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation, the patients were allocated to five groups: (1) normal controls (eGFR ≥90 mL/min/1.73 m2 without pathologic, urine [proteinuria], blood [electrolyte], and imaging abnormalities; n = 22); (2) CKD stage 2 (eGFR 60–89 mL/min/1.73 m2; n = 17); (3) CKD stage 3 (eGFR 30–59 mL/min/1.73 m2; n = 22); (4) CKD stage 4 (eGFR 15–30 mL/min/1.73 m2; n = 17); and (5) CKD stage 5-hemodialysis (HD) (n = 30). All the patients were free of clinically apparent cardiovascular disease. Serum FGF-23, elastase, lactoferrin, and angiogenin concentrations and the MPR were measured to study the association of the above parameters with the clinical (age, sex, presence of diabetes mellitus, and blood pressure), biochemical (calcium, phosphorus, uric acid, intact parathyroid hormone [PTH], low-density lipoprotein cholesterol, and high-sensitivity C-reactive protein), and ba-PWV values of the CKD patients. Results: (1) The mean ba-PWV values were 1,497.2 ± 206.4 cm/s in the controls, 1,649.0 ± 247.9 cm/s in the CKD stage 2 group (p < 0.05 vs. controls), 1,655.8 ± 260.3 cm/s in the CKD stage 3 group (p < 0.05 vs. controls), 1,823.0 ± 402.4 cm/s in the CKD stage 4 group (p < 0.05 vs. controls and CKD stages 2 and 3), and 1,905.2 ± 374.1 cm/s in the CKD stage 5-HD group (p < 0.05 vs. controls and CKD stage 2). (2) The mean log10(FGF-23) concentration values were 0.77 ± 0.27, 0.97 ± 0.48, 1.10 ± 0.35 (p < 0.05 vs. controls and CKD stage 2), 1.35 ± 0.48 (p < 0.05 vs. controls and CKD stages 2 and 3), and 2.12 ± 0.82 (p < 0.05 vs. controls and CKD stages 2–4); the mean angiogenin levels were 230.6 ± 70.5 pg/mL, 283.0 ± 53.5 pg/mL (p < 0.05 vs. controls), 347.3 ± 76.9 pg/mL (p < 0.05 vs. controls and CKD stage 2), 445.9 ± 90.6 pg/mL (p < 0.05 vs. controls and CKD stages 2 and 3), and 370.9 ± 142.4 pg/mL (p < 0.05 vs. controls and CKD stages 2 and 3). (3) In the stage 3–4 CKD/HD patients, the mean elastase-to-neutrophil and lactoferrin-to-neutrophil ratios were significantly lower than in the controls and the stage 2 CKD patients. (4) Our multivariate linear regression analyses showed that age, pulse pressure, mean arterial pressure, PTH, and FGF-23 were independently associated with ba-PWV values. Conclusions: Circulating FGF-23 and angiogenin concentrations gradually increased as CKD advanced, whereas neutrophil activation markers were significantly lower in the stage 3–4 CKD/HD patients than in the controls and stage 2 CKD patients. FGF-23 was weakly associated with ba-PWV values in patients with CKD/HD and no previous cardiovascular disease.

Download Full-text