Disease ⇒ Chronic kidney disease {40000186}

Record Keys

Parent:[  ]
Chronic kidney disease


Initialisation date:
Other Terms:

Meta Information

MedDra ID:
MedDra Level:
ICD:[  ]
Zone:[  ]
Mechanism:[  ]


[  ]

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

[  ]

Common References

MetaBiom only uses strictly necessary session cookies to give you the best possible experience on the website. By selecting "Accept essential cookies" you agree to the use of these cookies.