scholarly journals A Pilot Study of a Natural Food Supplement as New Possible Therapeutic Approach in Chronic Kidney Disease Patients

2020 ◽  
Vol 13 (7) ◽  
pp. 148 ◽  
Author(s):  
Annalisa Noce ◽  
Alessio Bocedi ◽  
Margherita Campo ◽  
Giulia Marrone ◽  
Manuela Di Lauro ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
High Performance ◽  
Glutathione Transferase ◽  
Food Supplement ◽  
Array Detector ◽  
Natural Food ◽  
Inflammatory Status

The identification of natural bioactive compounds, able to counteract the abnormal increase of oxidative stress and inflammatory status in chronic degenerative non-communicable diseases is useful for the clinical management of these conditions. We tested an oral food supplement (OFS), chemically characterized and evaluated for in vitro and in vivo activity. Vitamin C, analyzed by High Performance Liquid Chromatography-Diode Array Detector (HPLC-DAD), was 0.19 mg/g in rosehip dry extract and 15.74 mg/capsule in the OFS. The identification of polyphenols was performed by HPLC-DAD; the total antioxidant capacity was assessed by Folin–Ciocalteu test. Total polyphenols were 14.73 mg/g gallic acid equivalents (GAE) for rosehip extract and 1.93 mg/g GAE for OFS. A total of 21 chronic kidney disease (CKD) patients and 10 healthy volunteers were recruited. The evaluation of routine laboratory and inflammatory parameters, erythrocyte glutathione transferase (e-GST), human oxidized serum albumin (HSAox), and assessment of body composition were performed at two different times, at baseline and after 5 weeks of OFS assumption. In the study, we highlighted a significant decrease of traditional inflammatory biomarkers (such as C-reactive protein, erythrocyte sedimentation rate, platelet to lymphocyte ratio) and other laboratory parameters like e-GST, azotaemia, and albuminuria after OFS treatment in CKD patients. Moreover, we demonstrated a lipid profile improvement in CKD patients after OFS supplementation.

scholarly journals Mitochondrial Targeting of Herbal Medicine in Chronic Kidney Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Qing Li ◽  
Changying Xing ◽  
Yanggang Yuan
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Herbal Medicine ◽  
Mitochondrial Function ◽  
Conventional Medicine ◽  
Treatment Options ◽  
Renal Diseases ◽  
Public Health Issue

Chronic kidney disease (CKD) is a common progressive disease that is typically characterized by the permanent loss of nephrons and an eventual decline in glomerular filtration rate. CKD increases mortality and has a significant impact on the quality of life and the economy, which is becoming a major public health issue worldwide. Since current conventional-medicine treatment options for CKD are not satisfactory, many patients seek complementary and alternative medicine treatments including Traditional Chinese Medicine. Herbal medicine is often used to relieve symptoms of renal diseases in the clinic. The kidney is abundant in the number of mitochondria, which provide enough energy for renal function and metabolism. In recent years, a vital role for mitochondrial dysfunction has been suggested in CKD. Mitochondria have become a new target for the treatment of diseases. A growing number of studies have demonstrated herbal medicine could restore mitochondrial function and alleviate renal injury both in vivo and in vitro. In this review, we sum up the therapeutic effect of herbal medicine in CKD via targeting mitochondrial function. This implies future strategies in preventing CKD.

scholarly journals Possible Prophylactic Effect of Poria Mushroom Extract on Chemically-Induced Chronic Kidney Disease In Vitro and In Vivo

2019 ◽  
Vol 4 (10) ◽  
Author(s):  
Jonathan Wagmaister ◽  
Kelvin Zheng ◽  
Muhammad Choudhury ◽  
Majid Eshghi ◽  
Sensuke Konno
Keyword(s):  
Chronic Kidney Disease ◽  
Antioxidant Activity ◽  
Kidney Disease ◽  
Cell Viability ◽  
Prophylactic Effect ◽  
Renal Cells ◽  
Mushroom Extract ◽  
Rat Kidneys

Background: Hypothesizing that oxidative stress (OXS) could be a key pathogenic factor for the incidence of chronic kidney disease (CKD), we investigated if the Poria mushroom extract, PE, with possible antioxidant activity, would prevent the incidence of CKD in rats. Materials and Methods: Antioxidant activity of PE was examined against OXS induced by hydrogen peroxide (H2O2) in renal LLC-PK1 cells. Whether PE could prevent the development of CKD in the rat kidneys, mediated through adenine (ADN)-induced OXS, was also examined. After 2 weeks, blood and kidney specimens were collected from rats for blood, histopathologic, and biochemical analyses. Results: Although H2O2-induced OXS led to a significant cell viability reduction in LLC-PK1 cells, PE significantly diminished OXS and sustained high (~70%) cell viability. In rats, ADN-given rats showed typical renal dysfunction with palpable kidney damage; however, PE supplement improved renal function with better histology. A ~2.2-fold increased OXS level was also seen in ADN-given rats but it was reduced by ~27% with PE supplement. Moreover, analysis of kidney injury biomarkers further confirmed extended kidney damage by ADN. Nevertheless, PE effectively maintained the natural status of those markers, protecting the rat kidneys. Conclusions: OXS is indeed harmful to renal cells in vitro and could even lead to ADN-induced CKD in vivo. However, PE appears to have antioxidant activity capable of protecting renal cells and the rat kidneys from such detrimental OXS. Therefore, it is rather possible that PE could be a natural antioxidant with prophylactic effect against OXS-induced CKD.

scholarly journals Quantitative Translation of Microfluidic Transporter in Vitro Data to in Vivo Reveals Impaired Albumin-Facilitated Indoxyl Sulfate Secretion in Chronic Kidney Disease

2019 ◽  
Vol 16 (11) ◽  
pp. 4551-4562 ◽  
Author(s):  
Thomas K. van der Made ◽  
Michele Fedecostante ◽  
Daniel Scotcher ◽  
Amin Rostami-Hodjegan ◽  
Javier Sastre Toraño ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Indoxyl Sulfate ◽  
Vitro Data ◽  
In Vitro Data

scholarly journals The Pathophysiologic Role of Gelsolin in Chronic Kidney Disease: Focus on Podocytes

2021 ◽  
Vol 22 (24) ◽  
pp. 13281
Author(s):  
Chia-Jung Yu ◽  
Dian W. Damaiyanti ◽  
Shian-Jang Yan ◽  
Chih-Hsing Wu ◽  
Ming-Jer Tang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Critical Role ◽  
Physiological Role ◽  
Small Gtpase ◽  
Common Finding ◽  
Puromycin Aminonucleoside ◽  
Filtration Barrier

Chronic kidney disease (CKD) is normally related to proteinuria, a common finding in a compromised glomerular filtration barrier (GFB). GFB is a structure composed of glomerular endothelial cells, the basement membrane, and the podocytes. CKD with podocyte damage may be associated with actin cytoskeleton reorganization, resulting in podocyte effacement. Gelsolin plays a critical role in several diseases, including cardiovascular diseases and cancer. Our current study aimed to determine the connection between gelsolin and podocyte, and thus the mechanism underlying podocyte injury in CKD. Experiments were carried out on Drosophila to demonstrate whether gelsolin had a physiological role in maintaining podocyte. Furthermore, the survival rate of gelsolin-knocked down Drosophila larvae was extensively reduced after AgNO3 exposure. Secondly, the in vitro podocytes treated with puromycin aminonucleoside (PAN) enhanced the gelsolin protein expression, as well as small GTPase RhoA and Rac1, which also regulated actin dynamic expression incrementally with the PAN concentrations. Thirdly, we further demonstrated in vivo that GSN was highly expressed inside the glomeruli with mitochondrial dysfunction in a CKD mouse model. Our findings suggest that an excess of gelsolin may contribute to podocytes damage in glomeruli.

scholarly journals Exogenous Wnt1 Prevents Acute Kidney Injury and Its Subsequent Progression to Chronic Kidney Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Xue Hong ◽  
Yanni Zhou ◽  
Dedong Wang ◽  
Fuping Lyu ◽  
Tianjun Guan ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Blood Biochemical

Studies suggest that Wnt/β-catenin agonists are beneficial in the treatment of acute kidney injury (AKI); however, it remains elusive about its role in the prevention of AKI and its progression to chronic kidney disease (CKD). In this study, renal Wnt/β-catenin signaling was either activated by overexpression of exogenous Wnt1 or inhibited by administration with ICG-001, a small molecule inhibitor of β-catenin signaling, before mice were subjected to ischemia/reperfusion injury (IRI) to induce AKI and subsequent CKD. Our results showed that in vivo expression of exogenous Wnt1 before IR protected mice against AKI, and impeded the progression of AKI to CKD in mice, as evidenced by both blood biochemical and kidney histological analyses. In contrast, pre-treatment of ICG-001 before IR had no effect on renal Wnt/β-catenin signaling or the progression of AKI to CKD. Mechanistically, in vivo expression of exogenous Wnt1 before IR suppressed the expression of proapoptotic proteins in AKI mice, and reduced inflammatory responses in both AKI and CKD mice. Additionally, exogenous Wnt1 inhibited apoptosis of tubular cells induced by hypoxia-reoxygenation (H/R) treatment in vitro. To conclude, the present study provides evidences to support the preventive effect of Wnt/β-catenin activation on IR-related AKI and its subsequent progression to CKD.

scholarly journals Interleukin-1α (IL-1α) is a Central Regulator of Leukocyte-Endothelial Adhesion in Myocardial Infarction and in Chronic Kidney Disease

Circulation ◽  
2021 ◽  
Author(s):  
Stefan J. Schunk ◽  
Sarah Triem ◽  
David Schmit ◽  
Stephen Zewinger ◽  
Tamim Sarakpi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Chronic Kidney Disease ◽  
Endothelial Cells ◽  
Kidney Disease ◽  
Cell Types ◽  
Surface Expression ◽  
Organ Injury ◽  
Underlying Mechanisms

Background: Cardiovascular diseases (CVD) and chronic kidney disease (CKD) are highly prevalent, aggravate each other, and account for substantial mortality. Both conditions are characterized by activation of the innate immune system. The alarmin IL-1α is expressed in a variety of cell types promoting (sterile) systemic inflammation. The aim of the present study was to examine the role of IL-1α in mediating inflammation in the setting of acute myocardial infarction (AMI) and CKD. Methods: We assessed the expression of IL-1α on the surface of monocytes from patients with AMI and patients with CKD and determined its association with atherosclerotic CVD events during follow-up in an explorative clinical study. Furthermore, we assessed the inflammatory effects of IL-1α in several organ injury models in Il1a -/- and Il1b -/- mice and investigated the underlying mechanisms in vitro in monocytes and endothelial cells. Results: IL-1α is strongly expressed on the surface of monocytes from patients with AMI and CKD compared to healthy controls. Higher IL-1α surface expression on monocytes from patients with AMI and CKD was associated with a higher risk for atherosclerotic CVD events, which underlines the clinical relevance of IL-1α. In mice, IL-1α, but not IL-1β, mediates leukocyte-endothelial adhesion as determined by intravital microscopy. IL-1α promotes accumulation of macrophages and neutrophils in inflamed tissue in vivo . Furthermore, IL-1α on monocytes stimulates their homing at sites of vascular injury. A variety of stimuli such as free fatty acids or oxalate crystals induce IL-1α surface expression and release by monocytes, which then mediates their adhesion to the endothelium via IL-1 receptor-1. Besides, IL-1α promotes expression of the vascular cell adhesion molecule-1 (VCAM-1) on endothelial cells thereby fostering the adhesion of circulating leukocytes. IL-1α induces inflammatory injury after experimental AMI and abrogation of IL-1α prevents the development of CKD in oxalate or adenine-fed mice. Conclusions: IL-1α represents a key mediator of leukocyte-endothelial adhesion and inflammation in AMI and CKD. Inhibition of IL-1α may serve as a novel anti-inflammatory treatment strategy.

scholarly journals Human uraemic serum displays calcific potential in vitro that increases with advancing chronic kidney disease

2013 ◽  
Vol 125 (5) ◽  
pp. 237-245 ◽  
Author(s):  
Ashish Patidar ◽  
Dhruv K. Singh ◽  
Peter Winocour ◽  
Ken Farrington ◽  
Anwar R. Baydoun
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Serum Creatinine ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Therapeutic Strategies ◽  
High Morbidity ◽  
Kidney Impairment

Vascular calcification (VC) strongly correlates with declining renal function and contributes to the high morbidity and mortality of patients with CKD (chronic kidney disease). It is closely regulated by circulating factors but little is known about the capacity of serum from patients to induce calcification outside the disease setting, which we now define as the calcific potential of serum. We have therefore examined the ability of serum from age- and sex-matched subjects with and without advancing CKD to induce calcification of cultured SMCs (smooth muscle cells). Samples from patients with CKD induced significant calcification compared with controls. More importantly, samples from patients on haemodialysis induced significantly higher calcification than those with moderate or advanced CKD. The calcification induced by the latter two but not those on haemodialysis could be enhanced with calcium chloride and β-GP (β-glycerophosphate). A positive correlation was evident between measured serum creatinine, phosphate, PTH (parathyroid hormone), OPG (osteoprotegerin) and the degree of calcification in vitro. eGFR (estimated glomerular filtration rate), DBP (diastolic blood pressure), haemoglobin and serum albumin correlated negatively. Stepwise multivariate analysis of log-transformed calcific potential data highlighted serum creatinine, albumin and OPG as significant predictors, explaining approximately 50% of the variation. Thus, other regulators, either not investigated or as yet unidentified, may contribute to the calcification potential of serum in vitro. Furthermore, uraemic serum can induce graded calcification outside of the disease milieu that reflects the degree of kidney impairment in vivo. These findings could have important clinical relevance in terms of developing novel diagnostic and/or therapeutic strategies for subjects with CKD.

scholarly journals SHROOM3, the gene associated with chronic kidney disease, affects the podocyte structure

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ryo Matsuura ◽  
Atsuko Hiraishi ◽  
Lawrence B. Holzman ◽  
Hiroki Hanayama ◽  
Koji Harano ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Kidney Function ◽  
Genome Wide Association Study ◽  
Kidney Diseases ◽  
Vitro Experiment ◽  
Public Health Burden ◽  
In Vitro Experiment

AbstractChronic kidney disease is a public health burden and it remains unknown which genetic loci are associated with kidney function in the Japanese population, our genome-wide association study using the Biobank Japan dataset (excluding secondary kidney diseases, such as diabetes mellitus) clearly revealed that almost half of the top 50 single nucleotide polymorphisms associated with estimated glomerular filtration rate are located in the SHROOM3 gene, suggesting that SHROOM3 will be responsible for kidney function. Thus, to confirm this finding, supportive functional analyses were performed on Shroom3 in mice using fullerene-based siRNA delivery, which demonstrated that Shroom3 knockdown led to albuminuria and podocyte foot process effacement. The in vitro experiment shows that knockdown of Shroom3 caused defective formation of lamellipodia in podocyte, which would lead to the disruption of slit diaphragm. These results from the GWAS, in vivo and in vitro experiment were consistent with recent studies reporting that albuminuria leads to impairment of kidney function.

scholarly journals Adipokines as a link between obesity and chronic kidney disease

2013 ◽  
Vol 305 (12) ◽  
pp. F1629-F1636 ◽  
Author(s):  
Jessica F. Briffa ◽  
Andrew J. McAinch ◽  
Philip Poronnik ◽  
Deanne H. Hryciw
Keyword(s):  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Cell Types ◽  
Peripheral Tissues ◽  
Increased Risk

Adipocytes secrete a number of bioactive adipokines that activate a variety of cell signaling pathways in central and peripheral tissues. Obesity is associated with the altered production of many adipokines and is linked to a number of pathologies. As an increase in body weight is directly associated with an increased risk for developing chronic kidney disease (CKD), there is significant interest in the link between obesity and renal dysfunction. Altered levels of the adipokines leptin, adiponectin, resistin, and visfatin can decrease the glomerular filtration rate and increase albuminuria, which are pathophysiological changes typical of CKD. Specifically, exposure of the glomerulus to altered adipokine levels can increase its permeability, fuse the podocytes, and cause mesangial cell hypertrophy, all of which alter the glomerular filtration rate. In addition, the adipokines leptin and adiponectin can act on tubular networks. Thus, adipokines can act on multiple cell types in the development of renal pathophysiology. Importantly, most studies have been performed using in vitro models, with future studies in vivo required to further elucidate the specific roles that adipokines play in the development and progression of CKD.

scholarly journals Molecular Mechanistic Pathways Targeted by Natural Antioxidants in the Prevention and Treatment of Chronic Kidney Disease

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 15
Author(s):  
Mohamed Mohany ◽  
Mohammed M. Ahmed ◽  
Salim S. Al-Rejaie
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Transforming Growth Factor Beta ◽  
Clinical Studies ◽  
Transforming Growth Factor ◽  
Related Factor ◽  
Nuclear Factor ◽  
Kidney Fibrosis

Chronic kidney disease (CKD) is the progressive loss of renal function and the leading cause of end-stage renal disease (ESRD). Despite optimal therapy, many patients progress to ESRD and require dialysis or transplantation. The pathogenesis of CKD involves inflammation, kidney fibrosis, and blunted renal cellular antioxidant capacity. In this review, we have focused on in vitro and in vivo experimental and clinical studies undertaken to investigate the mechanistic pathways by which these compounds exert their effects against the progression of CKD, particularly diabetic nephropathy and kidney fibrosis. The accumulated and collected data from preclinical and clinical studies revealed that these plants/bioactive compounds could activate autophagy, increase mitochondrial bioenergetics and prevent mitochondrial dysfunction, act as modulators of signaling pathways involved in inflammation, oxidative stress, and renal fibrosis. The main pathways targeted by these compounds include the canonical nuclear factor kappa B (NF-κB), canonical transforming growth factor-beta (TGF-β), autophagy, and Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid factor 2-related factor 2 (Nrf2)/antioxidant response element (ARE). This review presented an updated overview of the potential benefits of these antioxidants and new strategies to treat or reduce CKD progression, although the limitations related to the traditional formulation, lack of standardization, side effects, and safety.

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