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The glomerulus and Bowman's capsule are two essential components of the nephron, which is the functional unit of the kidney. These microscopic structures play a critical role in the process of blood filtration to produce urine.
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A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
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Uremic Toxins, CKD, and Cognitive Dysfunction.

Taylor D Andrews1,2, Gregory S Day3, Sarosh R Irani3,4

  • 1Department of Neurosciences, Mayo Clinic Graduate School Biomedical Sciences, Mayo Clinic, Jacksonville, Florida.

Journal of the American Society of Nephrology : JASN
|February 26, 2025
PubMed
Summary
This summary is machine-generated.

Cognitive impairment is common in chronic kidney disease (CKD), especially kidney failure. Research is advancing on the kidney-brain axis, exploring toxins, brain injury, and new therapies to improve cognitive function in CKD patients.

Keywords:
ApoECKD nondialysisESKDbiomarkersdementiadialysisimagingtransplantationuremia

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Area of Science:

  • Nephrology
  • Neurology
  • Neuroscience

Background:

  • Cognitive impairment affects 20-70% of individuals with chronic kidney disease (CKD), significantly higher than the general population.
  • Kidney failure and dialysis-dependent patients exhibit a doubled prevalence of cognitive impairment compared to age-matched controls.
  • Recent research on the
  • kidney-brain axis
  • has rapidly expanded, investigating CKD-related cognitive dysfunction mechanisms and treatments.

Purpose of the Study:

  • To review recent literature on the direct and indirect effects of CKD-associated cognitive impairment.
  • To emphasize the roles of uremic toxins, brain injury mechanisms, and the overlap with neurodegenerative diseases like Alzheimer's.
  • To summarize reviewed therapeutic interventions and suggest future research directions.

Main Methods:

  • Literature review focusing on translational studies of CKD-associated brain injury.
  • Examination of in vitro and in vivo models to understand pathogenic processes like oxidative stress, neuroinflammation, and blood-brain barrier dysfunction.
  • Analysis of therapeutic interventions including AST-120, CH-223191, triarylmethane-34, anakinra, marimastat, exercise, supplements, and kidney transplantation.

Main Results:

  • CKD-associated cognitive impairment involves uremic toxins, oxidative stress, neuroinflammation, and blood-brain barrier dysfunction.
  • Therapeutic strategies reviewed show potential for mitigating CKD-related cognitive decline.
  • Significant knowledge gaps remain, necessitating further scientific advancement.

Conclusions:

  • CKD-associated cognitive impairment is a prevalent condition requiring targeted research and therapeutic development.
  • Future research should explore senotherapeutics and regenerative cell-based therapies for their anti-inflammatory effects.
  • Preserving cognitive function in CKD patients is crucial for improving their quality of life.