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Kidney Structure01:45

Kidney Structure

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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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Acute Kidney Injury I: Introduction01:22

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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...
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Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

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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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Acute Kidney Injury V: Interprofessional Care01:20

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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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Acute Kidney Injury VI: Nursing Management01:22

Acute Kidney Injury VI: Nursing Management

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Acute Kidney Injury (AKI) results in an inability to maintain fluid, electrolyte, and acid-base balance. Effective nursing management is critical in improving patient outcomes and includes comprehensive patient assessment and targeted interventions.Comprehensive Patient AssessmentA detailed history collection is essential, focusing on any recent infections, nephrotoxic medication use, or chronic conditions such as hypertension and diabetes that may contribute to AKI. During the physical...
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Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

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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...
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Related Experiment Video

Updated: Jan 23, 2026

A Quantitative Detection Method for MicroRNAs in the Kidney of an Ischemic Kidney Injury Mouse Model
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A Quantitative Detection Method for MicroRNAs in the Kidney of an Ischemic Kidney Injury Mouse Model

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Renal Ketogenesis Protects Against Ischemic Kidney Injury.

Kyle Feola1, Andrea H Venable1, Mina Rasouli1

  • 1Department of Internal Medicine (Nephrology) and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas.

Journal of the American Society of Nephrology : JASN
|January 22, 2026
PubMed
Summary
This summary is machine-generated.

Kidney Hydroxymethylglutaryl-CoA synthase 2 (HMGCS2) plays a protective role in acute kidney injury by supporting fatty acid oxidation. Loss of kidney HMGCS2 worsens injury and impairs mitochondrial function, highlighting its importance in renal health.

Keywords:
AKImetabolism

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Last Updated: Jan 23, 2026

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Area of Science:

  • Nephrology
  • Metabolic pathways
  • Mitochondrial function

Background:

  • Dysregulated metabolism, specifically fatty acid oxidation, is implicated in kidney disease.
  • Mitochondrial Hydroxymethylglutaryl-CoA synthase 2 (HMGCS2), the rate-limiting enzyme for ketogenesis, is induced in kidney proximal tubules during fasting.
  • Kidney-specific HMGCS2 does not contribute to systemic ketone levels but may act locally.

Purpose of the Study:

  • To investigate the local role of kidney HMGCS2 in maintaining renal function during metabolic stress or injury.
  • To determine if kidney HMGCS2 protects against ischemia-reperfusion injury (IRI).

Main Methods:

  • Mice with kidney-specific Hmgcs2 deletion were subjected to IRI.
  • Kidney histology, metabolomics, and lipidomics were analyzed.
  • Mitochondrial fatty acid oxidation capacity was measured in proximal tubular mitochondria.

Main Results:

  • Kidney-specific Hmgcs2 deletion exacerbated IRI, leading to increased kidney injury.
  • Loss of HMGCS2 resulted in decreased kidney ketone content and increased lipid droplet accumulation.
  • Mitochondria lacking HMGCS2 showed reduced fatty acid oxidation capacity post-IRI.
  • A ketogenic diet mitigated kidney injury and improved mitochondrial function in Hmgcs2 knockout mice.

Conclusions:

  • Renal HMGCS2 is crucial for limiting ischemia-induced acute kidney injury.
  • Loss of renal HMGCS2 impairs mitochondrial fatty acid oxidation and exacerbates kidney injury.
  • Targeting renal ketogenesis may offer a therapeutic strategy for acute kidney injury.