Disease ⇒ Chronic kidney disease {40000186}

Shared Reference Notes

• [1.1] 
  - In chronic kidney disease (CKD), the “healthy” microbiota structure is disrupted, and intestinal microbes produce large quantities of uremic solutes responsible for renal damage; on the other hand, the uremic state, fueled by reduced renal clearance, causes shifts in microbial metabolism and composition, hence creating a vicious cycle in which dysbiosis and renal dysfunction are progressively worsened.
• [1.2] 
  - Saccharibacteria (per 1-SD higher in the log-transformed abundance) could potentially decrease the concentration of serum creatinine and increase the estimated glomerular filtration rate which might help improve renal function.
• [1.3] [#Uremic toxins] 
• [1.4] 
  - #Curcumin > significantly reduced plasma pro-inflammatory mediators (CCL-2, IFN-γ, and IL-4) and lipid peroxidation. - After 6 months of #Curcumin supplementation > significantly lower #Escherichia-#Shigella and significantly higher #Lachnoclostridium . - In the last 3 months of supplementation > significantly higher #Lactobacillaceae spp..
• [1.5] 
  - Bacterial species involved in #Butyrate production, #Indole synthesis and mucin degradation were also related to CKD.
• [1.6] 
  - Chronic kidney disease > decreased #Indole, #Indole-3-carboxaldehyde and #Indole-3-propionic acid
• [1.7] [#Aging] 
  - #Hippuric acid has been found increased in patients with chronic kidney disease and several age-related conditions
• [1.8] 
• [1.9] 
  - #Hydrogen sulfide (H2S) and methanethiol are produced during the decomposition of #Sulfur-containing amino acids, and have been linked to the progression of chronic kidney disease (CKD), cardiovascular disease, and bone metabolic disorders
• - #Butyrate can protect glomerular endothelial cells against mitochondrial dysfunction.
• [#Short Chain Fatty Acid] - fecal and serum SCFAs are remarkably higher in healthy controls than in patients affected by CKD. - the progression of CKD negatively correlates with the amount of #Butyrate detected in the serum of the patients. - #Butyrate supplementation might have potential beneficial effects on kidney function
• - In CKD patients, the concentrations of microbiota-derived trimethylamine N-oxide (#TMAO), indoxyl #Sulfate and p-cresyl #Sulfate in the blood are increased. Because of poor renal function in CKD patients, these #Uremic toxins remain in the circulation, promote inflammation, thereby contributing to progressive kidney injury.
• [1.11] [#Phenylacetylglutamine] 
  - high plasma levels of PAG have been observed in patients with chronic kidney disease.
• [#Phenylacetylglutamine] - patients with chronic kidney disease (CKD) circulating PAG was found to be associated with risk of future #CVD
• [1.12] 
  - #TMAO causes kidney injury and tubulointerstitial #Fibrosis. - Higher #TMAO levels associated with higher risk of incident CKD and greater annualized eGFR decline, and with monotonic dose-response relationships.
• [1.13] 
  - #TMAO was also able to significantly induce #IL-6 release alone from renal fibroblast, strengthening the link to renal #Fibrosis.
• [#TNF-alfa] - combined exposure of #TMAO and TNF-α can increase fibronectin release from renal fibroblasts. - Several studies indicate that #TMAO exacerbates tubulointerstitial #Fibrosis and renal inflammation in CKD. - neither #TMAO nor TNF-α alone increased fibronectin release from renal fibroblasts. - #TMAO and TNF-α alone or in combination increased total collagen production. - the combination of #TMAO and TNF-α can increase fibronectin release compared to TNF-α alone. - Fibronectin, a high molecular weight glycoprotein with adhesive properties, holds a pivotal function in both wound-healing processes and the formation of extracellular matrix - TNF-α and #TMAO induced increased fibroblast proliferation and that the combination of TNF-α 1 ng/ml and #TMAO induced increased cell proliferation compared to TNF-α alone. - both #TMAO and TNF-α mediate their proliferative and collagen inducing effects on renal fibroblast via Akt, mTOR and ERK, but not PI3K.
• - #TMAO can reduce megalin expression in proximal tubular cells via PI3K and ERK

References Notes