scholarly journals A Pilot Randomized Crossover Trial Assessing the Safety and Short-Term Effects of Walnut Consumption by Patients with Chronic Kidney Disease

2019 ◽  
Author(s):  
Pilar Sanchis ◽  
Marilisa Molina ◽  
Francisco Berga ◽  
Elena Muñoz ◽  
Regina Fortuny ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Dietary Supplement ◽  
Cardiovascular Events ◽  
Inositol Phosphates ◽  
Control Diet ◽  
Fibroblast Growth Factor 23 ◽  
Short Term ◽  
Daily Consumption

The aim of this study of patients with chronic kidney disease (CKD) is to assess the safety of daily consumption of walnuts on the physiological levels of phosphorous, potassium, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23), and to assess the short-term benefits of this intervention on risk factors associated with cardiovascular events. This led us to perform a prospective, randomized, cross-over, pilot clinical trial examined 13 patients with chronic kidney disease (CKD). Subjects were randomly assigned to a diet of 30 g of walnuts per day or the control diet. After 30 days, each group was given a 30-day washout period, and then switched to the alternate diet for 30 days. Urinary and serum levels of phosphorous and potassium, multiple vascular risk factors, and urinary inositol phosphates (InsPs) were measured at baseline and at the end of the intervention period. Our results showed that the walnut dietary supplement led to reduced blood pressure, LDL cholesterol, and serum albumin, but had no effect on the physiological levels of phosphorous, potassium, PTH, and FGF23. This is the first report to show that daily consumption of walnuts by patients with CKD does not alter their physiological levels of phosphorous, potassium, PTH, and FGF23. Consequently, this dietary supplement may prevent cardiovascular events in patients with CKD.

scholarly journals A Pilot Randomized Crossover Trial Assessing the Safety and Short-Term Effects of Walnut Consumption by Patients with Chronic Kidney Disease

Nutrients ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 63 ◽  
Author(s):  
Pilar Sanchis ◽  
Marilisa Molina ◽  
Francisco Berga ◽  
Elena Muñoz ◽  
Regina Fortuny ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Inositol Phosphates ◽  
Control Diet ◽  
Fibroblast Growth Factor 23 ◽  
Serum Levels ◽  
Short Term ◽  
Daily Consumption ◽  
Randomized Crossover Trial

The aim of this study of patients with chronic kidney disease (CKD) is to assess the safety of daily consumption of walnuts on the physiological levels of phosphorous, potassium, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23), and to assess the short-term benefits of this intervention on risk factors associated with cardiovascular events. This led us to perform a prospective, randomized, crossover, pilot clinical trial examined 13 patients with CKD. Subjects were randomly assigned to a diet of 30 g of walnuts per day or the control diet. After 30 days, each group was given a 30-day washout period, and then switched to the alternate diet for 30 days. Urinary and serum levels of phosphorous and potassium, multiple vascular risk factors, and urinary inositol phosphates (InsPs) were measured at baseline and at the end of the intervention period. Our results showed that the walnut dietary supplement led to reduced blood pressure, LDL cholesterol, and albumin excretion, but had no effect on the physiological levels of phosphorous, potassium, PTH, and FGF23. This is the first report to show that daily consumption of walnuts by patients with CKD does not alter their physiological levels of phosphorous, potassium, PTH, and FGF23 when included in a sodium-, protein-, phosphate-, and potassium-controlled diet, and it could be an effective strategy for reducing cardiovascular risk in patients with CKD.

Strength of Fibroblast Growth Factor 23 as a Cardiovascular Risk Predictor in Chronic Kidney Disease Weaken by ProBNP Adjustment

2019 ◽  
Vol 49 (3) ◽  
pp. 203-211 ◽  
Author(s):  
Insa E. Emrich ◽  
Vincent Brandenburg ◽  
Alexander B. Sellier ◽  
Johanna Schauerte ◽  
Johanna Wiedenroth ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Cardiovascular Events ◽  
Fibroblast Growth Factor 23 ◽  
Cardiovascular Effects ◽  
Fibroblast Growth ◽  
Conventional Risk Factors

Background: Various epidemiological studies linked high fibroblast growth factor 23 (FGF23) levels with cardiovascular events in chronic kidney disease (CKD). It remains enigmatic whether high FGF23 exerts adverse cardiovascular effects, or whether it reflects detrimental effects of residual confounders. Earlier studies adjusted for CKD-mineral bone disease (CKD-MBD) regulators of FGF23 rather than for recently discovered non-CKD-MBD regulators, among which iron deficiency and heart failure are of particular importance. Moreover, they used c-terminal FGF23 (cFGF23) assays rather than more specific intact FGF23 (iFGF23) assays. Methods: The CARE FOR HOMe study analyzed plasma ferritin, iFGF23, cFGF23 and N-terminal proBNP (NT-proBNP) along with conventional risk factors, among 575 CKD G2-G4 patients to determine the interaction between FGF23, its non-CKD-MBD regulators, and incident cardiovascular events in CKD patients. The participants were followed up for 5.1 ± 2.1 years for the occurrence of atherosclerotic events and hospitalization for acute decompensated heart failure. Results: cFGF23 correlated strongly with high iFGF23 (r = 0.607), fairly with high NT-proBNP (r = 0.453) and weakly with low ferritin (r = –0.207); correlation coefficients of iFGF23 with NT-proBNP and ferritin were numerically lower. In Kaplan-Meier analyses, both endpoints were predicted by cFGF23 and iFGF23. In Cox regression models, cFGF23 remained an outcome predictor after adjustment for conventional risk factors and ferritin. This prediction was largely eliminated when further adjusting for NT-proBNP. iFGF23 was less consistently associated with adverse outcome in partly adjusted models, and failed to predict outcome in fully adjusted models. Conclusion: In summary, iron deficiency and heart failure affect plasma FGF23. As adjustment for NT-proBNP virtually eliminates the association between plasma FGF23 and predefined outcome, we speculate that high FGF23, rather than exerting detrimental cardiovascular effects, mirrors prevalent heart disease.

Cardiovascular Protection With Sodium-Glucose Cotransporter-2 Inhibitors and Mineralocorticoid Receptor Antagonists in Chronic Kidney Disease

Hypertension ◽  
2021 ◽  
Vol 77 (5) ◽  
pp. 1442-1455
Author(s):  
Pantelis Sarafidis ◽  
Christodoulos E. Papadopoulos ◽  
Vasilios Kamperidis ◽  
George Giannakoulas ◽  
Michael Doumas
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cardiovascular Events ◽  
Mineralocorticoid Receptor ◽  
Mineralocorticoid Receptor Antagonists ◽  
Receptor Antagonists ◽  
Cardiovascular Protection ◽  
Sodium Glucose Cotransporter

Chronic kidney disease (CKD) and cardiovascular disease are intimately linked. They share major risk factors, including age, hypertension, and diabetes, and common pathogenetic mechanisms. Furthermore, reduced renal function and kidney injury documented with albuminuria are independent risk factors for cardiovascular events and mortality. In major renal outcome trials and subsequent meta-analyses in patients with CKD, ACE (angiotensin-converting enzyme) inhibitors and ARBs (angiotensin II receptor blockers) were shown to effectively retard CKD progression but not to significantly reduce cardiovascular events or mortality. Thus, a high residual risk for cardiovascular disease progression under standard-of-care treatment is still present for patients with CKD. In contrast to the above, several outcome trials with SGLT-2 (sodium-glucose cotransporter-2) inhibitors and MRAs (mineralocorticoid receptor antagonists) clearly suggest that these agents, apart from nephroprotection, offer important cardioprotection in this population. This article discusses existing evidence on the effects of SGLT-2 inhibitors and MRAs on cardiovascular outcomes in patients with CKD that open new roads in cardiovascular protection of this heavily burdened population.

Independent, Non-traditional Risk Factors for Cardiovascular Events and Atherothrombosis in Chronic Kidney Disease and in Hemodialysis-dependent Patients

2006 ◽  
Vol 6 (3) ◽  
pp. 484-491 ◽  
Author(s):  
Mona Ezzat Madkour . ◽  
Iman William Bekheet . ◽  
Nagwa Abdel-Ghaffar . ◽  
Emam Waked . ◽  
Khaled Younes .
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cardiovascular Events ◽  
Traditional Risk Factors

scholarly journals Short-term effects of sevelamer-carbonate on fibroblast growth factor 23 and pulse wave velocity in patients with normophosphataemic chronic kidney disease Stage 3

2019 ◽  
Vol 12 (5) ◽  
pp. 678-685 ◽  
Author(s):  
Annet Bouma-de Krijger ◽  
Frans J van Ittersum ◽  
Tiny Hoekstra ◽  
Pieter M ter Wee ◽  
Marc G Vervloet
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Pulse Wave Velocity ◽  
Fibroblast Growth Factor ◽  
Pulse Wave ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Short Term ◽  
Sevelamer Carbonate

Abstract Background High concentrations of both phosphate and fibroblast growth factor 23 (FGF23) observed in chronic kidney disease (CKD) are associated with an increased risk of cardiovascular morbidity and mortality. Pulse wave velocity (PWV) is a surrogate marker for cardiovascular events and all-cause mortality. It is not known whether a reduction of FGF23 or phosphate alters cardiovascular risk. Sevelamer has shown to have the ability to reduce both phosphate and FGF23 concentrations. Furthermore, reduction of PWV is reported with sevelamer use as well, but it is unclear if this is mediated by decline of phosphate or FGF23. We investigated if sevelamer induced a decline in PWV and if this was associated with a reduction in FGF23. Methods In all, 24 normophosphataemic CKD Stage 3 patients started treatment with a fixed dose of sevelamer-carbonate (Renvela®) 2.4 g twice daily, with their usual diet for 8 weeks in a single-arm study. PWV was measured and blood samples were obtained before, during and after washout of treatment with sevelamer. Vascular calcification was quantified using the Kauppila Index (KI). The primary outcome was the change of PWV from baseline to 8 weeks of treatment and the secondary endpoint was the difference of FGF23 following treatment with sevelamer. One of the linear mixed models was used to analyse the association between treatment and outcome. Mediation analysis was performed as a sensitivity analysis. The study was registered in the Dutch trial register (http://www.trialregister.nl: NTR2383). Results A total of 18 patients completed 8 weeks of treatment with sevelamer and were analysed. Overall, treatment with sevelamer did not induce a significant reduction of PWV (β = −0.36, P = 0.12). However, in patients with less vascular calcification (lower KI score), there was a statistically significant reduction of PWV, adjusted for mean arterial pressure, after treatment (β = 0.63, P = 0.02). Addition of FGF23 to the model did not alter this association. Mediation analysis yielded similar results. FGF23 did not decrease during treatment with sevelamer. Conclusion In this short-term pilot study in normophosphataemic CKD patients, treatment with sevelamer did not improve PWV. In subgroup analysis, however, PWV improved in patients with no or limited abdominal aorta calcifications. This was not associated with a decline of FGF23.

P5526Vascular endothelial growth factor-D and mortality in suspected or known coronary heart disease patients with chronic kidney disease: a subanalysis of the ANOX study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Wada ◽  
M Suzuki ◽  
M Matsuda ◽  
Y Ajiro ◽  
T Shinozaki ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Coronary Angiography ◽  
Cardiovascular Events ◽  
Cardiovascular Death ◽  
Endothelial Growth Factor

Abstract Background Chronic kidney disease (CKD) is an independent risk factor for the development and progression of coronary heart disease (CHD). Vascular endothelial growth factor-D (VEGF-D) is a secreted glycoprotein that can act as lymphangiogenic and angiogenic growth factors through binding to its specific receptors, VEGFR-3 (Flt-4) and VEGFR-2 (KDR/Flk-1). VEGF-D signaling via VEGFR-3 plays an important role in lipoprotein metabolisms which may contribute to CHD. VEGF-D signaling has been used as a therapeutic target of human diseases such as lymphangioleiomyomatosis and refractory angina. Furthermore, in clinical settings, the VEGF-D level is already established as a diagnostic biomarker for lymphangioleiomyomatosis. However, the prognostic value of VEGF-D in suspected or known CHD patients with CKD is unknown. Methods Serum VEGF-D levels were measured in 999 suspected or known CHD patients with CKD undergoing elective coronary angiography, enrolled in the development of novel biomarkers related to angiogenesis or oxidative stress to predict cardiovascular events (ANOX) study, and followed up for 3 years. The primary outcome was all-cause death. The secondary outcomes were cardiovascular death, and major adverse cardiovascular events (MACE) defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke. Results During the follow-up, 154 patients died from any cause, 61 died from cardiovascular disease, and 96 developed MACE. After adjustment for established risk factors, VEGF-D levels were significantly associated with all-cause death (hazard ratio [HR] for 1-SD increase, 1.41; 95% confidence interval [CI], 1.27–1.56), cardiovascular death (HR, 1.48; 95% CI, 1.28–1.71), and MACE (HR, 1.34; 95% CI, 1.18–1.53). Even after incorporation of N-terminal pro-brain natriuretic peptide, contemporary sensitive cardiac troponin-I, and high-sensitivity C-reactive protein into a model with established risk factors, the addition of VEGF-D levels further improved the prediction of all-cause death (continuous net reclassification improvement [NRI], 0.272; 95% CI, 0.100–0.445; P=0.002; integrated discrimination improvement [IDI], 0.015; 95% CI, 0.003–0.027; P=0.013), but not that of cardiovascular death (NRI, 0.230; 95% CI, −0.029 to 0.488; P=0.082; IDI, 0.012; 95% CI, −0.007 to 0.031; P=0.207) or MACE (NRI, 0.102; 95% CI, −0.106 to 0.310; P=0.337; IDI, 0.005; 95% CI, −0.005 to 0.015; P=0.337). Conclusions In suspected or known CHD patients with CKD undergoing elective coronary angiography, elevated VEGF-D levels may predict all-cause mortality independent of established risk factors and cardiovascular biomarkers. Acknowledgement/Funding The ANOX study is supported by a Grant-in-Aid for Clinical Research from the National Hospital Organization

scholarly journals Fibroblast growth factor 23 and new-onset chronic kidney disease in the general population: the Prevention of Renal and Vascular Endstage Disease (PREVEND) study

2020 ◽  
Vol 36 (1) ◽  
pp. 121-128 ◽  
Author(s):  
Maarten A De Jong ◽  
Michele F Eisenga ◽  
Adriana J van Ballegooijen ◽  
Joline W J Beulens ◽  
Marc G Vervloet ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Population Based ◽  
Fibroblast Growth ◽  
Fgf23 Level ◽  
Increased Risk ◽  
All Cause Mortality ◽  
New Onset

Abstract Background Fibroblast growth factor 23 (FGF23), a phosphate-regulating hormone that increases early in the course of chronic kidney disease (CKD), is associated with disease progression in patients with established CKD. Here we aimed to investigate the association between plasma FGF23 and new-onset CKD in the general population. Methods We included 5253 individuals without CKD who participated in the Prevention of Renal and Vascular Endstage Disease study, a prospective, population-based cohort. Multi-variable Cox regression was used to study the association of plasma C-terminal FGF23 with new-onset CKD, defined as a combined endpoint of estimated glomerular filtration rate (eGFR) <60 mL/min/ 1.73 m2, urinary 24-h albumin excretion (UAE) >30 mg/24 h or both, or with all-cause mortality. Results The median baseline FGF23 was 68 [interquartile range (IQR) 56–85] RU/mL, eGFR was 95 ± 13 mL/min/1.73 m2 and UAE was 7.8 (IQR 5.8–11.5)  mg/24 h. After follow-up of 7.5 (IQR 7.2–8.0)  years, 586 participants developed CKD and 214 participants died. A higher FGF23 level was associated with new-onset CKD, independent of risk factors for kidney disease and parameters of bone and mineral homoeostasis {fully adjusted hazard ratio (HR) 1.25 [95% confidence interval (CI) 1.10–1.44] per doubling of FGF23; P = 0.001}. In secondary analyses, FGF23 was independently associated with new-onset eGFR <60 mL/min/1.73 m2 [adjusted HR 1.28 (95% CI 1.00–1.62); P = 0.048] or with UAE >30 mg/24 h [adjusted HR 1.24 (95% CI 1.06–1.45); P = 0.01] individually. A higher FGF23 level was also associated with an increased risk of all-cause mortality [fully adjusted HR 1.30 (95% CI 1.03–1.63); P = 0.03]. Conclusions High FGF23 levels are associated with an increased risk of new-onset CKD and all-cause mortality in this prospective population-based cohort, independent of established CKD risk factors.

scholarly journals Novel Cardiovascular Risk Factors in Patients with Diabetic Kidney Disease

2021 ◽  
Vol 22 (20) ◽  
pp. 11196
Author(s):  
Christodoula Kourtidou ◽  
Maria Stangou ◽  
Smaragdi Marinaki ◽  
Konstantinos Tziomalos
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Risk Stratification ◽  
Cardiovascular Risk Factors ◽  
Cardiovascular Events ◽  
Diabetic Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Diabetic Kidney ◽  
Increased Risk

Patients with diabetic kidney disease (DKD) are at very high risk for cardiovascular events. Only part of this increased risk can be attributed to the presence of diabetes mellitus (DM) and to other DM-related comorbidities, including hypertension and obesity. The identification of novel risk factors that underpin the association between DKD and cardiovascular disease (CVD) is essential for risk stratification, for individualization of treatment and for identification of novel treatment targets.In the present review, we summarize the current knowledge regarding the role of emerging cardiovascular risk markers in patients with DKD. Among these biomarkers, fibroblast growth factor-23 and copeptin were studied more extensively and consistently predicted cardiovascular events in this population. Therefore, it might be useful to incorporate them in risk stratification strategies in patients with DKD to identify those who would possibly benefit from more aggressive management of cardiovascular risk factors.

scholarly journals P0765RHEUMATOID ARTHRITIS AND CHRONIC KIDNEY DISEASE: DOES INFLAMMATION SAY IT ALL?

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Marina Sofia Rodrigues Reis ◽  
Pedro Salvador ◽  
Ana Marta Gomes ◽  
Sara Beça ◽  
João Carlos Fernandes
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cardiovascular Events ◽  
Estimated Glomerular Filtration Rate ◽  
Mortality And Morbidity ◽  
American College Of Rheumatology ◽  
Increase Risk ◽  
Independent Risk Factors ◽  
The Mean

Abstract Background and Aims Rheumatoid arthritis (RA) increase risk of developing chronic kidney disease (CKD), but it is unknow which risk factors contributes to CKD in this population. This study aims to determine predictors for the development of CKD in RA patients. Method A retrospective study was conducted in 106 patients with RA followed at a sub-specialized internal medicine appointment between January 2007 and December 2017. RA was defined according to the American College of Rheumatology criteria and CKD was defined as an estimated glomerular filtration rate less than 60mL/min/ 1.73m2 or presence of abnormalities of urinary sediment for 3 months. Results The mean age was 61 ± 12.83 years, and 67.9% (n=72) were female. The prevalence of CKD was 20.8% (n=22). Renal disease had multifactorial etiology in 20 patients, and one case of ANCA negative glomerulonephritis and other of diabetic nephropathy. Individuals with RA and CKD were older, presented more cardiovascular disease, diabetes and hypertension. There was no statistically significant association between gender and the presence of CKD (p = 0.131). Age (p = 0.031) and diabetes (p = 0.031) were independent risk factors for development of CKD in RA patients. RA duration in patients with CKD (8, 4-13) was not statistically different from RA duration in non-CKD patients (7.50, 4,75 – 12,25), (p=0.890). Conclusion Patients with RA and CKD had higher incidence of cardiovascular events, diabetes and hypertension which are a major cause of mortality and morbidity in this group. The presence of diabetes mellitus that often arise as an adverse effect of drugs used in the treatment of RA, significantly increased the risk of developing CKD. Otherwise, RA duration didn’t represent a risk factor for developing CKD. Thus, it is important to control diabetes, particularly glucocorticoid-induced diabetes to prevent development of CKD in AR patients.

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