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Related Concept Videos

Chronic Kidney Disease II: Clinical Manifestations01:24

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Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
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Chronic Kidney Disease I: Introduction01:25

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Chronic Kidney Disease (CKD) arises when the kidneys progressively lose their ability to function, ultimately leading to end-stage renal disease. At this advanced stage, the kidneys can no longer filter waste or maintain essential body functions, requiring renal replacement therapy (RRT) through dialysis or a kidney transplant for survival.Early-stage chronic kidney disease and detection challengesIn CKD's early stages, symptoms often remain absent because healthy nephrons compensate for...
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Acute Kidney Injury II: Pathophysiology01:29

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Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
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Renal dysfunction significantly impairs the renal clearance of drugs, leading to potential complications in drug therapy. Renal failure, which can be caused by various factors, poses a significant challenge in the elimination of drugs from the body.
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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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In patients with renal impairment, drugs undergo significant changes in their pharmacokinetics, which require dosage adjustments to ensure safe and effective therapy.
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Assessment of Vascular Function in Patients With Chronic Kidney Disease
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Mitochondrial stress and glycoxidation increase with decreased kidney function.

Nana Katsuta1, Mime Nagai2, Kaishi Saruwatari2

  • 1Laboratory of Food and Regulation Biology, Graduate School of Bioscience, Tokai University, Toroku 9-1-1, Higashi-ku, Kumamoto 862-8652, Japan.

Journal of Clinical Biochemistry and Nutrition
|March 20, 2023
PubMed
Summary

Mitochondrial stress elevates fumarate, leading to increased S-(2-succinyl)cysteine and advanced glycation end-products (AGEs) in chronic kidney disease (CKD). Levels decreased post-transplant, suggesting S-(2-succinyl)cysteine as a biomarker for kidney metabolic changes.

Keywords:
S-(2-succinyl)cysteineadvanced glycation end-productschronic kidney diseasefumaratekidney transplantation

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Area of Science:

  • Biochemistry
  • Metabolomics
  • Nephrology

Background:

  • Mitochondrial stress elevates fumarate, a Krebs cycle intermediate.
  • Fumarate reacts with cysteine to form S-(2-succinyl)cysteine.
  • Advanced glycation end-products (AGEs) are associated with metabolic dysfunction.

Purpose of the Study:

  • Quantify fumarate, S-(2-succinyl)cysteine, and AGEs in chronic kidney disease (CKD) patients.
  • Evaluate metabolite differences between healthy individuals and kidney transplant recipients.
  • Assess metabolite changes longitudinally after kidney transplantation.

Main Methods:

  • Liquid chromatography-tandem mass spectrometry (LC-MS/MS) for metabolite quantification.
  • Enzymatic assay for specific metabolite measurements.
  • Cross-sectional and longitudinal study designs involving CKD, end-stage renal disease (ESRD), and kidney transplant patients.

Main Results:

  • S-(2-succinyl)cysteine and AGEs levels were elevated in CKD patients and decreased significantly post-transplant.
  • Fumarate levels were significantly different only in ESRD patients.
  • S-(2-succinyl)cysteine levels correlated with kidney function markers.

Conclusions:

  • Mitochondrial metabolic dysfunction contributes to impaired kidney function in CKD.
  • S-(2-succinyl)cysteine shows potential as a minimally invasive biomarker for metabolic changes in CKD.
  • Kidney transplantation improves metabolic derangements associated with CKD.