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.

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.

MO566THE BONE EXPRESSION OF WNT INHIBITORS IN THE EXPERIMENTAL MODEL OF EARLY CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Evdokia Bogdanova ◽  
Natalia Semenova ◽  
Olga Galkina ◽  
Irina Zubina ◽  
Olga Beresneva ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Experimental Model ◽  
Inorganic Phosphate ◽  
Molecular Mechanisms ◽  
Fibroblast Growth Factor 23 ◽  
Bone Matrix ◽  
Serum Levels ◽  
Chow Diet ◽  
Dickkopf 1

Abstract Background and Aims Molecular mechanisms implicated in the initial stages of inorganic phosphate (Pi) imbalance in chronic kidney disease (CKD) remain poorly understood.The aim of the study was to evaluate whether canonical Wnt pathway inhibitors (iWnt) involved in early response to Pi retention in CKD. Methods Mild CKD was induced by 3/4 nephrectomy (NE) in spontaneously hypertensive rats (SHR) fed rat chow diet containing 0.6 % phosphate. Controls were sham operated SHR (SO). Duration of experimental exposure (NE or SO) was 2 and 6 months. Serum levels of creatinine (Cr), inorganic phosphate (Pi), fractional Pi excretion (FEPi), intact parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), alfa-Klotho (KL), sclerostin (SOST) and Dickkopf-1 (DKK1) were measured. The following morphological characteristics by light microscopy of bone metaphysis and kidney tissues: the area of renal interstitial fibrosis (RF) (Masson's trichrome), bone matrix volume (MV), the active osteoblasts to trabecular cells number ratio (aOB/cells), eroded surface to bone surface ratio (ES/BS) (hematoxylin & eosin), and bone SOST and DKK1 proteins expression (by IHC) were analyzed and calculated quantitatively. Statistical comparisons among groups were performed using Mann–Whitney U-test and Kruskal-Wallis H-test. Results Serum Cr, RF and indices of Pi exchange in the experimental model corresponded to early CKD (Table). Pi elevated in NE6 suggestive for its renal retention. KL level decreased (Table) in all experimental groups vs control. No differences were observed in serum levels FGF23 (p=0.62) and PTH (p=0.63). Serum SOST and DKK1 levels were significantly higher in NE6 group compared to SO6 (Table). The bone SOST and DKK1 expression increased in NE6 compared to SO6 (Figure). aOB/cells were lower in NE2, SO6 and NE6 vs SO2 (all p-values<=0.041). ES/BS increased in NE2 (vs SO2) while being lowest in NE6 and SO6 animals (Table). SOST and DKK1 metaphyseal expression increased in NE6 compared to SO2, SO6, NE2 (Figure). Osteocyte SOST expression increased in SO6 compared to SO2 and NE2 without differences in later groups. Osteoblast SOST expression was also higher in SO6 vs SO2 (Figure). Conclusion Increased serum levels of sclerostin and Dickkopf-1 and their bone expression are apparent in early stages of experimental CKD associating with hyperphosphatemia. Alterations of bone resorption and osteoblast depopulation occurred before the increase of serum Pi likely reflecting incipient stages of renal Pi retention. These molecular and cellular events seem to be independent of systemic FGF23 and PTH response.

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.

Pathophysiology of chronic kidney disease-mineral and bone disorder

2015 ◽  
Author(s):  
Alexandra Voinescu ◽  
Nadia Wasi Iqbal ◽  
Kevin J. Martin
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Serum Levels ◽  
Mineral And Bone Disorder ◽  
Vitamin D Metabolism ◽  
Bone Disorder ◽  
Calcium Phosphorus

Chronic kidney disease is associated with the inability to control normal mineral homeostasis, resulting in abnormalities in serum levels of calcium, phosphorus, parathyroid hormone, fibroblast growth factor 23 (FGF23) and vitamin D metabolism. These disturbances lead to the development of secondary hyperparathyroidism, skeletal abnormalities, vascular calcifications, and other systemic manifestations. Traditionally, mineral and bone abnormalities seen in chronic kidney disease were included in the term ‘renal osteodystrophy’. More recently, the term chronic kidney disease-mineral and bone disorder was introduced to define the biochemical abnormalities of phosphorus, parathyroid hormone, FGF23, calcium, or vitamin D metabolism, abnormalities in bone remodelling and mineralization, and vascular or other soft tissue calcifications.

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 The Kidney and COVID-19: Pandemic Effects on the Patients

2020 ◽  
Vol 10 (6) ◽  
pp. X1-X2
Author(s):  
A.S.M. Sarwar ◽  
Divya Jain ◽  
Anika Bushra ◽  
Khandaker Sabit Bin Razzak ◽  
Mohammad Nabil Hossain ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Respiratory Failure ◽  
Kidney Disease ◽  
Chronic Renal Disease ◽  
Diffuse Alveolar Damage ◽  
Serum Levels ◽  
Principal Characteristics ◽  
Patient Health

COVID-19 pathogens were identified as new coronaviruses by the sequencing of sample lower respiratory tracts from patients affected, which share a sequence of 79.6 percent identified as severe acute respiratory syndrome coronavirus. The virus has spread rapidly worldwide and was reported as a pandemic on 11 March 2020 since its detection in Wuhan, China in December 2019. The principal characteristics of COVID-19 were diffuse alveolar damage and acute respiratory failure, involving other organs. Although co-morbidities such as diabetes and cardiovascular disease have reported as risk factors of COVID-19, there is still no proof of an increased vulnerability to chronic renal disease in patients with chronic kidney disease (CKDs), although there are several studies continuing worldwide. CKD is differentiated by kidney structure abnormalities or functions which last > 3 months and have an impact on patient health. The deaths were not specifically caused by COVID-19, but were considered systemic causes. In HD patients with COVID-19 there were decreased lymphopenia, reduced serum levels of inflammatory receptors and more severe clinical disease than patients with HD CKD. Therefore, additional precautions should be taken in CKD patients to minimize risk of the infection. Doctors can also be carefully watched to identify signs of worsening of the disease in CKD patients with confirmed COVID-19.

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.

The Change of Serum FGF-23 Levels Predicts the Progression of Renal Function in Chronic Kidney Disease Patients

2020 ◽  
Vol 103 (11) ◽  
pp. 1155-1162
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Renal Function ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Positive Association ◽  
Ckd Progression ◽  
Fgf 23

Background: The role of elevated baseline fibroblast growth factor 23 (FGF-23) levels on the progression of renal function in long term (years) follow-up studies is not yet established. Objective: To circumvent the confounding factors occurring during the study duration, the authors examined the roles of the changing values of FGF-23 and other risk factors on progression of renal function after a shorter term (months) follow-up. Materials and Methods: The present study was a 12-week prospective cohort study to determine the association between traditional and non-traditional risk factors on the progression of renal function. Results: Sixty-five chronic kidney disease (CKD) patients were included. After a 12-week follow-up, significant increases of serum creatinine, cystatin C, vitamin D level, and FGF-23 levels were observed. The delta FGF-23 values increased progressively according to the staging of the CKD. The baseline parathyroid hormone level, which was in the recommended range following the KDIGO guideline, and the delta FGF-23 values were the significant parameters that had association with the decline of the estimated glomerular filtration. There was a positive association between delta FGF-23 and delta 25-OH vitamin D values. Conclusion: The increasing change in serum FGF-23 level is significantly correlated with declining renal function. Thus, delta FGF-23 value could be utilized as a suitable biomarker for following and detecting CKD progression. Keywords: FGF-23, Vitamin D, CKD progression, Biomarker

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