A prospective study to evaluate the safety and efficacy of symbiotic supplementation (probiotic and prebiotic combination) in stage 5D chronic kidney disease patients

Background: Chronic Kidney Disease (CKD) is one of the major health disorders associated with significant morbidity and mortality. This was a 6 week’s interventional study of orally administered, symbiotic supplement (probiotic with prebiotic) in stage 5D patients of chronic kidney disease (CKD) on twice a week hemodialysis. The objective was to look for safety of symbiotics (Nitrophage ForteTM) and for its anti-inflammatory effects measured by serum hsCRP (Highly specific C reactive protein), IL-6 (Interleukin- 6) and TNF-α (Tumour Necrosis Factor- α) levels. This translating to improvement in the Quality of life (QOL) assessed using SF-36 QOL questionnaire and Subjective Global Assessment (SGA) scoring. Methods: Subjects on twice a week dialysis for at least 3 months were included. Parameters at baseline (representing previous 3 months) were compared to that at the end of treatment. Oral supplementation of strain specific and unique composition of symbiotic sachet supplementation were administered twice daily containing Lactobacillus acidophilus 400mg, Bifidobacterium longumm 400mg, Streptococcus thermophilus with Fructooligosaccharide 100mg adding to 1 gram was given for 6 weeks.Results: 38 patients out of total 48 enrolled completed the study. Symbiotic therapy was found to be well tolerated with no significant adverse effects. 60.52%, 55.26%, 44.7% of the patients had a decrease in hsCRP, TNF-α and IL-6 respectively. Among responders hsCRP and TNF-α showed significant decrease in levels from the baseline (p <0.05). Modified SF-36 QOL questionnaire mean score revealed significant improvement in general health (p < 0.05). Among secondary parameters renal biomarkers like urea, BUN and sodium showed statistically significant decrease (p <0.05).Conclusions: This study establishes the safety and anti-inflammatory efficacy of this symbiotic supplement. To our knowledge this is the first study looking at anti-inflammatory role of symbiotic in CKD 5D Patients. A placebo controlled, double blinded study with a larger sample size is warranted in future to further establish these findings.

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EVALUATION OF INFLAMMATION AND ENDOTHELIAL DYSFUNCTION BIOMARKERS IN CHRONIC KIDNEY DISEASE (CKD) PATIENTS IN SOKOTO, NIGERIA

Open Journal of Medical Research (ISSN: 2734-2093) ◽

10.52417/ojmr.v1i1.72 ◽

2021 ◽

Vol 1 (1) ◽

pp. 1-9

Author(s):

C. A. Otitolaiye ◽

D. M. Sahabi ◽

A. M. Makusidi ◽

Y. Saidu ◽

L. S. Bilbis

Keyword(s):

Chronic Kidney Disease ◽

Cardiovascular Diseases ◽

Endothelial Dysfunction ◽

Kidney Disease ◽

Progressive Increase ◽

Necrosis Factor Alpha ◽

Reactive Protein ◽

Cardiovascular Morbidity And Mortality ◽

Tnf Α ◽

Variable Equation

Inflammation and endothelial dysfunction have been known to be involved in the pathogenesis of cardiovascular diseases. As such, examining the levels of inflammation and endothelial dysfunction is very critical to the prevention of cardiovascular diseases among chronic kidney disease (CKD) patients. This study aimed to investigate the progression of inflammation and endothelial dysfunction among CKD patients in Sokoto. A total of 67 CKD patients were divided into 5 groups based on the stages of their kidney disease calculated using the MDRD 4-variable equation for estimated glomerular filtration rate (eGFR). The presence of inflammation was determined by C-Reactive Protein (CRP) and Tumor Necrosis Factor alpha, while endothelial dysfunction was determined by the levels of Asymmetric dimethylarginine (ADMA) using ELISA kits. The mean eGFR of the patients was 49.97 ± 4.69 ml/min/1.73m2. There was significant increase (p<0.05) in CRP, TNF-α and ADMA of the CKD patients across the stages as compared to the non-CKD subjects. It was observed that as the CRP, TNF-α and ADMA increase, the eGFR significantly (p<0.05) decreases. Both CRP and TNF-α indicated a significantly positive correlation (p<0.05) with ADMA. The results indicated progressive increase in inflammation and endothelial dysfunction as CKD deteriorates. In addition, increased levels of inflammation could directly affect endothelial dysfunction, thereby aggravating cardiovascular morbidity and mortality among CKD patients in Sokoto. Otitolaiye, C. A. | Department of Biochemistry, Sokoto State University, Sokoto, Nigeria

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Genetic Variants Associated with Chronic Kidney Disease in a Spanish Population

Scientific Reports ◽

10.1038/s41598-019-56695-2 ◽

2020 ◽

Vol 10 (1) ◽

Cited By ~ 1

Author(s):

Zuray Corredor ◽

Miguel Inácio da Silva Filho ◽

Lara Rodríguez-Ribera ◽

Antonia Velázquez ◽

Alba Hernández ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Resistance Index ◽

Nucleotide Polymorphisms ◽

C Reactive Protein ◽

Single Nucleotide ◽

Reactive Protein ◽

Tnf Α ◽

Physiological Pathways ◽

Comprehensive Study

AbstractChronic kidney disease (CKD) patients have many affected physiological pathways. Variations in the genes regulating these pathways might affect the incidence and predisposition to this disease. A total of 722 Spanish adults, including 548 patients and 174 controls, were genotyped to better understand the effects of genetic risk loci on the susceptibility to CKD. We analyzed 38 single nucleotide polymorphisms (SNPs) in candidate genes associated with the inflammatory response (interleukins IL-1A, IL-4, IL-6, IL-10, TNF-α, ICAM-1), fibrogenesis (TGFB1), homocysteine synthesis (MTHFR), DNA repair (OGG1, MUTYH, XRCC1, ERCC2, ERCC4), renin-angiotensin-aldosterone system (CYP11B2, AGT), phase-II metabolism (GSTP1, GSTO1, GSTO2), antioxidant capacity (SOD1, SOD2, CAT, GPX1, GPX3, GPX4), and some other genes previously reported to be associated with CKD (GLO1, SLC7A9, SHROOM3, UMOD, VEGFA, MGP, KL). The results showed associations of GPX1, GSTO1, GSTO2, UMOD, and MGP with CKD. Additionally, associations with CKD related pathologies, such as hypertension (GPX4, CYP11B2, ERCC4), cardiovascular disease, diabetes and cancer predisposition (ERCC2) were also observed. Different genes showed association with biochemical parameters characteristic for CKD, such as creatinine (GPX1, GSTO1, GSTO2, KL, MGP), glomerular filtration rate (GPX1, GSTO1, KL, ICAM-1, MGP), hemoglobin (ERCC2, SHROOM3), resistance index erythropoietin (SOD2, VEGFA, MTHFR, KL), albumin (SOD1, GSTO2, ERCC2, SOD2), phosphorus (IL-4, ERCC4 SOD1, GPX4, GPX1), parathyroid hormone (IL-1A, IL-6, SHROOM3, UMOD, ICAM-1), C-reactive protein (SOD2, TGFB1,GSTP1, XRCC1), and ferritin (SOD2, GSTP1, SLC7A9, GPX4). To our knowledge, this is the second comprehensive study carried out in Spanish patients linking genetic polymorphisms and CKD.

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Tumor Necrosis Factor (TNF-α) and C-reactive Protein (CRP) are Positively Associated with the Risk of Chronic Kidney Disease in Patients with Type 2 Diabetes

Yonsei Medical Journal ◽

10.3349/ymj.2010.51.4.519 ◽

2010 ◽

Vol 51 (4) ◽

pp. 519 ◽

Cited By ~ 30

Author(s):

Eun-Sil Yeo ◽

Ji-Yun Hwang ◽

Ji Eun Park ◽

Young Ju Choi ◽

Kap Bum Huh ◽

...

Keyword(s):

Type 2 Diabetes ◽

Chronic Kidney Disease ◽

Tumor Necrosis Factor ◽

Kidney Disease ◽

Tumor Necrosis ◽

C Reactive Protein ◽

Reactive Protein ◽

Tnf Α ◽

Necrosis Factor

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Genetic Variation in TNF-α, its Relation with Inflammatory Biomarkers and Susceptibility to Rheumatoid Arthritis

Annals of Immunology & Immunotherapy ◽

10.23880/aii-16000122 ◽

2020 ◽

Vol 2 (2) ◽

Author(s):

Khadiga Ahmed Ismail

Keyword(s):

Rheumatoid Arthritis ◽

Serum Level ◽

Functional Disability ◽

Serum Levels ◽

Amplification Refractory Mutation System ◽

Reactive Protein ◽

Tnf Α ◽

Mutation System ◽

Potential Factor ◽

Factor Α

Background: Tumor necrosis Factor-α (TNF-α) is encoded and controlled by TNF-α gene, which is involved in rheumatoid arthritis (RA) susceptibility. This research aimed to identify genetic variations of TNF-α (G308A) and to establish its association with inflammatory markers in Rheumatoid Arthritis predisposition. Methods: In the present study, fifty RA patients and fifty volunteers were involved and evaluated for the C-reactive protein, rheumatoid factor, and TNF-α were estimated by ELISA, Erythrocyte Sedimentation Rate (ESR) by Wintergreen method and for TNF-α-308 G>A polymorphism by polymerase chain reaction with amplification refractory mutation system (PCR-ARMS). Results: The CRP, RF, ESR and TNF-α were significantly elevated in RA patients relative to controls. The serum level TNF-α was also significantly elevated in female patients and in patients ≥50 years. Analysis of TNF-308 gene polymorphism revealed that GG genotypes were more prevalent in RA patients than in the healthy individuals and that GG genotype may be a potential factor to RA. The G allele was more common in RA than in the control. Elevated TNF-α serum levels were significantly associated the GG genotype and functional disability in RA patients. Conclusion: TNF-α promoter 308polymorphism GG genotype may be considered as a risk factor for RA and the TNF-α serum level was significantly related to the functional disability in the disease.

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Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽

10.3390/molecules25163573 ◽

2020 ◽

Vol 25 (16) ◽

pp. 3573

Author(s):

Lian-Chun Li ◽

Zheng-Hong Pan ◽

De-Sheng Ning ◽

Yu-Xia Fu

Keyword(s):

Nitric Oxide ◽

Signaling Pathway ◽

Morphological Changes ◽

Raw264.7 Cells ◽

Enzyme Linked Immunosorbent Assay ◽

Tnf Α ◽

Anti Inflammatory ◽

Factor Α ◽

Oxide Synthase ◽

Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

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Temporal evolution of C-reactive protein levels and its association with the incident hospitalization risk among individuals with stage 3–4 chronic kidney disease

International Urology and Nephrology ◽

10.1007/s11255-021-02935-2 ◽

2021 ◽

Author(s):

Koray Uludag ◽

Gulsah Boz ◽

Tamer Arikan ◽

Ali Ihsan Gunal

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Temporal Evolution ◽

C Reactive Protein ◽

Protein Levels ◽

Reactive Protein

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Anti-Allergic and Anti-Inflammatory Effects of Undecane on Mast Cells and Keratinocytes

Molecules ◽

10.3390/molecules25071554 ◽

2020 ◽

Vol 25 (7) ◽

pp. 1554

Author(s):

Dabin Choi ◽

Wesuk Kang ◽

Taesun Park

Keyword(s):

Mast Cells ◽

Cyclic Adenosine Monophosphate ◽

Adenosine Monophosphate ◽

Allergic Diseases ◽

Intracellular Camp ◽

Tnf Α ◽

Anti Inflammatory ◽

Skin Conditions ◽

Factor Α ◽

Camp Levels

The critical roles of keratinocytes and resident mast cells in skin allergy and inflammation have been highlighted in many studies. Cyclic adenosine monophosphate (cAMP), the intracellular second messenger, has also recently emerged as a target molecule in the immune reaction underlying inflammatory skin conditions. Here, we investigated whether undecane, a naturally occurring plant compound, has anti-allergic and anti-inflammatory activities on sensitized rat basophilic leukemia (RBL-2H3) mast cells and HaCaT keratinocytes and we further explored the potential involvement of the cAMP as a molecular target for undecane. We confirmed that undecane increased intracellular cAMP levels in mast cells and keratinocytes. In sensitized mast cells, undecane inhibited degranulation and the secretion of histamine and tumor necrosis factor α (TNF-α). In addition, in sensitized keratinocytes, undecane reversed the increased levels of p38 phosphorylation, nuclear factor kappaB (NF-κB) transcriptional activity and target cytokine/chemokine genes, including thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC) and interleukin-8 (IL-8). These results suggest that undecane may be useful for the prevention or treatment of skin inflammatory disorders, such as atopic dermatitis, and other allergic diseases.

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