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Related Concept Videos

Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

49
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...
49
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

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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 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...
58
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

53
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...
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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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Related Experiment Video

Updated: Aug 17, 2025

3D Ultrasound Imaging: Fast and Cost-effective Morphometry of Musculoskeletal Tissue
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Activin A level is associated with physical function in critically ill patients.

Yi Tian Wang1, Craig A Harrison2, Elizabeth H Skinner3

  • 1School of Primary and Allied Health Care, Monash University, Melbourne, Australia; Department of Physiotherapy, Peninsula Health, Melbourne, Australia.

Australian Critical Care : Official Journal of the Confederation of Australian Critical Care Nurses
|December 14, 2022
PubMed
Summary

Elevated activin A levels in critically ill patients correlate with reduced muscle strength and physical function upon hospital discharge. Higher peak activin A may predict functional decline, suggesting its potential as a therapeutic target.

Keywords:
ActivinsICU-acquired weaknessMortalityMuscleSarcopeniaSkeletal

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Area of Science:

  • Intensive Care Medicine
  • Muscle Physiology
  • Biochemistry

Background:

  • Activin A is a known negative regulator of muscle mass.
  • Elevated activin A levels are observed in critical illness.
  • The association between activin A and physical function in critically ill patients remains unclear.

Purpose of the Study:

  • To investigate the relationship between serum activin A levels and muscle strength.
  • To examine the association between serum activin A levels and physical function.
  • To assess these relationships at intensive care unit (ICU) and hospital discharge.

Main Methods:

  • Thirty-six critically ill patients from two tertiary ICUs were recruited.
  • Participants required mechanical ventilation >48 hours and ICU stay >5 days.
  • Serum activin A levels were measured daily; muscle strength and physical function (e.g., Six-Minute Walk Test) were assessed at discharge.

Main Results:

  • Higher peak activin A levels were significantly associated with a worse Six-Minute Walk Test distance at hospital discharge.
  • No significant associations were found between peak activin A concentration and secondary outcome measures of muscle strength and physical function.

Conclusions:

  • Elevated peak activin A may be linked to functional decline in critically ill patients.
  • Further research is warranted to explore activin A as a therapeutic target.
  • Activin A could serve as a prospective predictor for muscle wasting in critical illness.