The Association of Fibroblast Growth Factor 23 with Arterial Stiffness and Atherosclerosis in Patients with Autosomal Dominant Polycystic Kidney Disease

Çoban, Melahat; İnci, Ayça; Yılmaz, Üstün; Asilturk, Emre

doi:10.1159/000492244

Cited by 16 publications

(16 citation statements)

References 38 publications

(51 reference statements)

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“…Furthermore, exposure to FGF23-which is a growth factor-triggers hypertrophy in isolated rat myocardiocytes [122]. Accordingly, high circulating levels of this bone hormone correlate with impaired endothelium-dependent vasodilation [123], increased arterial stiffness [124], and left ventricular hypertrophy [125] in CKD patients. However, the implication of high FGF23 for CV diseases remains unclear.…”

Section: The Endothelium In Ckdmentioning

confidence: 99%

Endothelial Dysfunction in Chronic Kidney Disease, from Biology to Clinical Outcomes: A 2020 Update

Roumeliotis

Mallamaci

Zoccali

2020

JCM

159

128

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The vascular endothelium is a dynamic, functionally complex organ, modulating multiple biological processes, including vascular tone and permeability, inflammatory responses, thrombosis, and angiogenesis. Endothelial dysfunction is a threat to the integrity of the vascular system, and it is pivotal in the pathogenesis of atherosclerosis and cardiovascular disease. Reduced nitric oxide (NO) bioavailability is a hallmark of chronic kidney disease (CKD), with this disturbance being almost universal in patients who reach the most advanced phase of CKD, end-stage kidney disease (ESKD). Low NO bioavailability in CKD depends on several mechanisms affecting the expression and the activity of endothelial NO synthase (eNOS). Accumulation of endogenous inhibitors of eNOS, inflammation and oxidative stress, advanced glycosylation products (AGEs), bone mineral balance disorders encompassing hyperphosphatemia, high levels of the phosphaturic hormone fibroblast growth factor 23 (FGF23), and low levels of the active form of vitamin D (1,25 vitamin D) and the anti-ageing vasculoprotective factor Klotho all impinge upon NO bioavailability and are critical to endothelial dysfunction in CKD. Wide-ranging multivariate interventions are needed to counter endothelial dysfunction in CKD, an alteration triggering arterial disease and cardiovascular complications in this high-risk population.

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Section: The Endothelium In Ckdmentioning

confidence: 99%

Endothelial Dysfunction in Chronic Kidney Disease, from Biology to Clinical Outcomes: A 2020 Update

Roumeliotis

Mallamaci

Zoccali

2020

JCM

159

128

View full text Add to dashboard Cite

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“…IMT represent an early marker of vascular dysfunction [21]. Several studies have shown higher IMT values in ADPK D than in healthy controls, even before the development of hypertension [22][23][24][25][26]. In our cohort, patients with ADPKD had the lowest IMT, while patients with ADPK D CKD stage 3 presented a similar IMT to controls.…”

Section: Discussionmentioning

confidence: 53%

Cardiovascular risk factors and the impact on prognosis in patients with chronic kidney disease secondary to autosomal dominant polycystic kidney disease

et al. 2021

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Background Autosomal dominant polycystic kidney disease (ADPKD) is the most frequent hereditary renal disease. There is an increased rate of cardiovascular disease (CVD) in ADPKD. In this study, we evaluate the prevalence of cardiovascular risk factors, the achievement rates for treatment goals and cardiovascular events (CVE) in ADPKD and their relations with asymptomatic CVD in CKD from other etiologies (CKDoe) and controls. Methods We evaluated 2445 CKD patients (2010–2012). The information collected was: clinical, anthropometric and analytical parameters, treatments and CVD evaluation (intima-media thickness (IMT), atheromatous plaque presence and ankle-brachial index (ABI)). Laboratory, vital status, CVE and hospitalizations were collected for 4 years. Results ADPKD patients had a worse renal function and worst achievement of blood pressure, higher parathormone levels but lower proteinuria compared to CKDoe. ADPKD patients presented lower IMT values than other groups, however, an intermediate rate of pathologic ABI and atheromatous plaque was present. More than half of the patients received statins, achieving LDL-c levels < 100 only in 50 and 39.8% of them (ADPKD and CKDoe respectively). The number of CVE during the follow-up period was low. In adjusted Cox regression model, ADPDK had the lowest occurrence of CVE of all three groups (HR:0.422, 95%CI 0.221–0.808, p = 0.009). Conclusion ADPKD patients show intermediate control rates of CVD. A better control of CVD risk seems to be related with a lower load of CVD compared to other groups, which may lead in the long term to a better prognosis. Further investigation is necessary to determine cardiovascular prognosis in ADPKD.

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“…Subsequently, five studies were excluded as two of them did not contain a control group, 29,30 two studies used different procedures for the evaluation of vascular stiffness 31,32 (ie nitroglycerin‐induced dilatation, hand skin heating test) while one article 33 represented a partial duplicate of a study that was already included in the present review. As a result, a total of 27 studies 34‐60 were included, comprising 1967 individuals (1141 ADPKD patients and 826 healthy controls).…”

Section: Resultsmentioning

confidence: 99%

Markers of endothelial dysfunction and arterial stiffness in patients with early‐stage autosomal dominant polycystic kidney disease: A meta‐analysis

2020

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Objectives Autosomal dominant polycystic kidney disease (ADPKD) is characterised by increased rates of cardiovascular complications leading to significant morbidity and mortality. This meta‐analysis aims to evaluate whether the disease is linked to endothelial dysfunction and arterial stiffness during its early stages. Methods Medline, Scopus, CENTRAL, Web of Science, Clinicaltrials.gov and Google Scholar databases comparing ADPKD patients with preserved renal function to healthy controls were included. The outcomes of interest were brachial flow‐mediated dilatation, carotid‐femoral pulse wave velocity, augmentation index, carotid intima‐media thickness and central systolic blood pressure, plasma ADMA or homocysteine levels. Standardised mean differences (SMDs) were estimated by a random‐effects model in R‐3.6.3. Results A total of 27 studies were included, comprising 1967 individuals. ADPKD was linked to significantly lower flow‐mediated dilatation (SMD: −1.44, 95% CI: [−2.35, −0.53]) and higher pulse wave velocity (SMD: 1.44, 95% CI: [0.22, 2.66]) and carotid intima‐media thickness (SMD: 1.02, 95% CI: [0.57, 1.47]). No significant associations were noted regarding augmentation index (SMD: 0.62, 95% CI: [−0.19, 1.43]) and central systolic blood pressure (SMD: 1.84, 95% CI: [−0.12, 3.80]). Plasma homocysteine was significantly higher in ADPKD (SMD: 0.81, 95% CI: [0.16, 1.45]), while no difference was calculated for ADMA levels (SMD: 1.14, 95% CI: [−0.25, 2.53]). Conclusions Early‐stage ADPKD patients present increased vascular stiffness and endothelial dysfunction, as reflected by low flow‐mediated dilatation and elevated values of pulse wave velocity, carotid intima‐media thickness and plasma homocysteine. The exact effects of early arterial stiffness on long‐term outcomes remain to be elucidated.

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The Association of Fibroblast Growth Factor 23 with Arterial Stiffness and Atherosclerosis in Patients with Autosomal Dominant Polycystic Kidney Disease

Cited by 16 publications

References 38 publications

Endothelial Dysfunction in Chronic Kidney Disease, from Biology to Clinical Outcomes: A 2020 Update

Endothelial Dysfunction in Chronic Kidney Disease, from Biology to Clinical Outcomes: A 2020 Update

Cardiovascular risk factors and the impact on prognosis in patients with chronic kidney disease secondary to autosomal dominant polycystic kidney disease

Markers of endothelial dysfunction and arterial stiffness in patients with early‐stage autosomal dominant polycystic kidney disease: A meta‐analysis

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