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Related Concept Videos

Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

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...
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
Renal Regulation of Acid-Base Balance01:29

Renal Regulation of Acid-Base Balance

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.
In the kidneys, cells within the proximal convoluted tubules (PCT) and the collecting ducts secrete hydrogen ions (H+) into the tubular fluid. Specifically, in the PCT, Na+/H+ antiporters secrete H+ while reabsorbing Na+.
However, the intercalated cells in...
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...
Acute Kidney Injury V: Interprofessional Care01:20

Acute Kidney Injury V: Interprofessional Care

Acute Kidney Injury (AKI) requires a collaborative healthcare approach to restore renal function and prevent complications. Essential management strategies involve monitoring fluid and electrolyte balance, adjusting medications, initiating dialysis when necessary, and providing nutritional support.Fluid and Electrolyte ManagementFluid Monitoring: Regularly monitoring body weight, central venous pressure, and urine output helps detect fluid imbalances early. Patient intake and output are...

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Noninvasive and Invasive Renal Hypoxia Monitoring in a Porcine Model of Hemorrhagic Shock
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Ozone oxidative post-conditioning in acute renal failure.

José Luis Calunga1, Yanelis Trujillo, Silvia Menéndez

  • 1Ozone International Clinic, Ozone Research Center, Havana, Cuba.

The Journal of Pharmacy and Pharmacology
|January 31, 2009
PubMed
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Ozone therapy significantly protected rat kidneys from warm ischaemia-reperfusion injury by upregulating antioxidant enzymes and improving renal function. This suggests ozone may minimize transplant-related renal damage.

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Area of Science:

  • Nephrology
  • Biochemistry
  • Oxidative Stress Research

Background:

  • Ischaemia-reperfusion injury is a major cause of kidney damage, largely mediated by reactive oxygen species.
  • Controlled ozone administration can enhance cellular antioxidant enzyme activity.

Purpose of the Study:

  • To investigate the protective effects of ozone therapy on renal function and morphology in rats subjected to warm renal ischaemia.
  • To evaluate the impact of ozone on biochemical markers of oxidative stress and renal function.

Main Methods:

  • Rats underwent 60 minutes of bilateral renal ischaemia followed by 10 days of reperfusion.
  • The ozone group received an ozone/oxygen mixture, while a control group received oxygen alone.
  • Biochemical parameters (fructosamine, phospholipase A2, catalase, superoxide dismutase, thiobarbituric acid reactive substances), renal plasma flow, and glomerular filtration rate were measured.

Main Results:

  • Ozone treatment preserved renal plasma flow and glomerular filtration rate, similar to controls.
  • Ozone administration increased catalase and superoxide dismutase activities, maintaining redox homeostasis.
  • Fewer morphological alterations were observed in ozone-treated kidneys compared to controls and oxygen-treated groups.

Conclusions:

  • Ozone therapy demonstrates a protective effect against renal ischaemia-reperfusion injury.
  • This protection is attributed to the upregulation of antioxidant defenses and improved oxygen metabolism.
  • Ozone may be a potential therapeutic strategy to mitigate renal damage post-transplantation.