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Urinary Tract Calculi III: Medical Management01:30

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The diagnosis of renal calculi involves several imaging techniques, including non-contrast CT scans and ultrasound. These methods help visualize kidney stones, assess their size and location, and detect possible obstructions. Additionally, Measuring urine pH is useful for diagnosing specific stone types, such as struvite (alkaline pH) and uric acid stones (acidic pH). Cystine stones are primarily linked to cystinuria, a genetic condition. A urinalysis helps detect blood in the urine (hematuria)...
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Urinary Tract Calculi II: Pathophysiology and Clinical Manifestations01:26

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Renal calculi, commonly termed kidney stones, are crystalline solid masses that form in the kidneys but can occur at any point within the urinary system, encompassing the kidneys, ureters, bladder, and urethra.The pathophysiology of renal stones involves several key factors: supersaturation of the urine with stone-forming constituents, changes in urine pH, a decrease in urine volume, and the presence of substances that promote or inhibit stone formation.Supersaturation of Urine: This is the...
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Urinary Tract Calculi IV: Nutrition Therapy and Prevention01:27

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Management of renal calculi focuses on effective strategies like tailored nutrition and hydration therapy. Adjusting diet and fluid intake reduces stone formation and recurrence, making these interventions simple yet powerful in kidney stone prevention and management.Understanding Kidney StonesKidney stones form when calcium, oxalate, uric acid, and cystine concentrate and crystallize in urine. Factors contributing to their formation include genetic predisposition, certain medical conditions,...
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The kidneys are intricate organs with millions of working units known as nephrons. Each nephron features two major structures: the renal corpuscle, which facilitates blood plasma filtration, and the renal tubule, which handles the glomerular filtrate. Blood supply is directly linked to the nephrons. The renal corpuscle consists of the glomerulus, a capillary network, and the Bowman's capsule, a double-walled epithelial structure that encases the glomerulus. The filtering of blood plasma...
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Urinary Tract Calculi I: Introduction01:28

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Renal calculi, or kidney stones, are solid deposits of minerals and salts formed inside the kidneys. In medical terminology, "calculus" refers to the stone itself, while "lithiasis" describes the process of stone formation. Depending on their location within the urinary system, these stones may be classified as either urolithiasis, when situated within the urinary tract, or nephrolithiasis, when located within the kidneys. Each term signifies the specific impact of the stone.Predisposition...
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The kidneys are two large bean-shaped organs located in the upper abdomen. They filter the blood several times a day to remove toxins and rebalance water and electrolytes of the circulatory system via the renal veins. The kidneys receive blood directly from the heart via the renal arteries. These arteries enter the kidney at the hilum, the concave surface of the bean, where they branch and divide into smaller vessels and capillaries.
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Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis
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Tight junction and kidney stone disease.

Papart Rungrasameviriya1, Aticha Santilinon1, Palita Atichartsintop1

  • 1Nawamethee Project, Doctor of Medicine Program, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.

Tissue Barriers
|May 10, 2023
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Summary

Defects in tight junctions (TJs) contribute to kidney stone disease (KSD). Targeting TJ pathways and genetic factors may offer new therapeutic strategies for preventing KSD.

Keywords:
Calcium oxalateROSSB239063TERZO-1claudinsdocetaxeloccludinphalloidin

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Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Medicine

Background:

  • Kidney stone disease (KSD) is a prevalent condition linked to epithelial dysfunction.
  • Tight junctions (TJs) are crucial for maintaining epithelial barrier integrity.
  • Defects in TJs are implicated in the pathogenesis of various diseases, including KSD.

Purpose of the Study:

  • To review the role of tight junction defects in kidney stone disease.
  • To summarize mechanisms of crystal-induced TJ damage in renal tubular epithelial cells (RTECs).
  • To discuss the impact of genetic variations in TJ proteins on KSD.

Main Methods:

  • Review of existing literature on KSD and TJ biology.
  • Analysis of signaling pathways (p38 MAPK, ROS/Akt/p38 MAPK) involved in crystal-induced TJ disruption.
  • Examination of F-actin reorganization and α-tubulin relocalization.
  • Investigation of genetic factors, including mutations and SNPs in CLDN genes.

Main Results:

  • Calcium oxalate (CaOx) crystals, particularly COM, disrupt TJs in RTECs.
  • Disruption occurs via p38 MAPK and ROS/Akt/p38 MAPK pathways, F-actin reorganization, and α-tubulin relocalization.
  • Pharmacological stabilization of TJ components (p38 MAPK, ROS, F-actin, α-tubulin) prevents COM-induced damage.
  • Genetic variations in CLDN2, CLDN10b, CLDN14, CLDN16, and CLDN19 are associated with KSD.

Conclusions:

  • Tight junction integrity is vital for preventing KSD.
  • Understanding TJ defect mechanisms provides insights into KSD pathogenesis.
  • Targeting TJs presents a promising therapeutic avenue for KSD prevention and treatment.