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Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

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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 (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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Chronic kidney disease (CKD) requires collaborative and comprehensive management. CKD progresses through stages and can lead to end-stage kidney disease (ESKD) if untreated. Interprofessional collaboration and patient education are crucial, enabling patients to manage their health and improve their quality of life.Diagnostic approach for chronic kidney diseaseThe diagnosis of CKD primarily focuses on the glomerular filtration rate (GFR), which assesses kidney function by measuring how well...
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A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro
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Mild Chronic Kidney Disease Associated with Low Bone Formation and Decrease in Phosphate Transporters and Signaling

Evdokia Bogdanova1, Airat Sadykov2, Galina Ivanova3

  • 1Research Institute of Nephrology, Pavlov University, 197022 Saint Petersburg, Russia.

International Journal of Molecular Sciences
|April 28, 2023
PubMed
Summary

Early chronic kidney disease (CKD) in rats showed lower bone turnover despite normal phosphate levels. Mild CKD induced maladaptive bone changes, affecting bone area, osteocyte, and osteoblast numbers, indicating reduced bone remodeling.

Keywords:
bone remodelingchronic kidney diseaseinorganic phosphate transportersintracellular signalingstatic bone histomorphometry

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Area of Science:

  • Nephrology
  • Bone Biology
  • Metabolic Bone Disease

Background:

  • Early chronic kidney disease (CKD) pathogenesis and its effects on bone are not fully understood.
  • Molecular and cellular bone responses in early CKD require further investigation.

Purpose of the Study:

  • To investigate the initial molecular and cellular bone responses in mild chronic kidney disease (CKD).
  • To analyze the impact of mild CKD on bone histomorphometry and gene expression profiles.

Main Methods:

  • Mild CKD was induced in spontaneously hypertensive rats (SHR) via hypertension or nephrectomy.
  • Bone histomorphometry, gene expression, and serum/urine markers (creatinine clearance, albumin-to-creatinine ratio, phosphate, PTH, FGF23, Klotho, Dickkopf-1, sclerostin) were assessed.

Main Results:

  • Mild CKD groups showed no increase in renal phosphate excretion, FGF23, or PTH.
  • Serum phosphate, Dickkopf-1, and sclerostin were elevated in the Nx6 group.
  • Histological analysis revealed decreased trabecular bone area, osteocyte, and osteoblast numbers in CKD groups.
  • Gene expression profiling indicated downregulation of Pi transport, MAPK, WNT, and BMP signaling pathways.

Conclusions:

  • Mild CKD is associated with histological and molecular changes indicative of lower bone turnover.
  • These bone alterations occur despite normal systemic phosphate-regulating factors.
  • The study highlights early maladaptive bone responses in mild CKD.