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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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Metabolic reactions in the body produce nonvolatile acids, such as sulfuric acid, which generate an acid load of approximately 1 mEq of H+ per kilogram of body weight daily. Excreting H+ in the urine is essential to balance this acid load.
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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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TRPV1 Hyperfunction Contributes to Renal Inflammation in Oxalate Nephropathy.

Chien-Lin Lu1,2, Te-Yi Teng3, Min-Tser Liao4

  • 1Division of Nephrology, Department of Medicine, Fu Jen Catholic University Hospital, New Taipei 24352, Taiwan.

International Journal of Molecular Sciences
|July 2, 2021
PubMed
Summary

Transient receptor potential vanilloid 1 (TRPV1) channel activation exacerbates kidney damage in hyperoxaluria. Inhibiting TRPV1 reduces inflammation and tubular injury, offering a potential therapeutic target for oxalate nephropathy.

Keywords:
12(S)-HETETRPV1arachidonate 12-lipoxygenasecalciumhyperoxaluriainflammasomeinflammationoxalateoxidative stress

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Inflammation Research

Background:

  • Inflammation exacerbates tubular damage in oxalate nephropathy.
  • The Transient Receptor Potential Vanilloid 1 (TRPV1) channel is expressed in the kidney and senses various stimuli.

Purpose of the Study:

  • To investigate the role of TRPV1 in hyperoxaluria-induced renal inflammation.
  • To determine if TRPV1 inhibition can attenuate oxalate nephropathy.

Main Methods:

  • Utilized TRPV1-expressing proximal tubular cells (LLC-PK1) and male hyperoxaluric rat models.
  • Assessed oxalate-induced cell damage, ALOX12 expression, endovanilloid synthesis, Ca2+ signaling, ROS production, and inflammatory markers (NLRP3, caspase-1, IL-1β).
  • Evaluated the effects of ALOX12 and TRPV1 inhibition on cellular and animal models.

Main Results:

  • Oxalate induced time- and dose-dependent cell damage, linked to ALOX12 expression and TRPV1 activation.
  • TRPV1 activation led to increased intracellular Ca2+, PKCα activation, NADPH oxidase 4 upregulation, ROS formation, and subsequent inflammation (NLRP3, caspase-1, IL-1β).
  • Inhibition of TRPV1 attenuated oxalate-mediated cell damage in vitro and significantly reduced tubular damage, oxidative stress, and crystal deposition in hyperoxaluric rats.

Conclusions:

  • TRPV1 hyperfunction contributes significantly to oxalate-induced renal inflammation and tubular injury.
  • Targeting and inhibiting TRPV1 function represents a promising therapeutic strategy to attenuate hyperoxaluric nephropathy.