Related Experiment Video

Updated: Jun 6, 2026

Mouse Model of Acute to Chronic Kidney Disease Transition Induced by Renal Ischemia/Reperfusion Injury
07:02

Mouse Model of Acute to Chronic Kidney Disease Transition Induced by Renal Ischemia/Reperfusion Injury

Published on: February 10, 2026

MCP-1 gene activation marks acute kidney injury

Raj Munshi1, Ali Johnson, Edward D Siew

  • 1Seattle Children’s Hospital Medical Center, Seattle, Washington, USA.

Journal of the American Society of Nephrology : JASN
|November 13, 2010
PubMed

Insights

Monocyte chemoattractant protein 1 (MCP-1) shows promise as a biomarker for acute kidney injury (AKI). Urinary MCP-1 levels were elevated in patients with AKI, suggesting its potential for diagnosing kidney damage.

Area of Science:

  • Nephrology
  • Biomarker Discovery
  • Molecular Biology

Background:

  • Monocyte chemoattractant protein 1 (MCP-1) is implicated in kidney injury.
  • The utility of MCP-1 as an acute kidney injury (AKI) biomarker remains unclear.
  • Neutrophil gelatinase-associated lipocalin (NGAL) is a known comparator AKI biomarker.

Purpose of the Study:

  • To investigate MCP-1's potential as a biomarker for AKI.
  • To compare MCP-1 with NGAL in various kidney injury models.
  • To explore urinary histone modifications as indicators of MCP-1 gene activation in AKI.

Main Methods:

  • Kidney and urine samples from mice with induced intrarenal, prerenal, and postrenal injury were analyzed.
  • Urine samples from critically ill patients with and without azotemia were assessed.
  • MCP-1, MCP-1 mRNA, NGAL, and histone marks (H3K4m3) at the MCP-1 gene were measured.

Main Results:

  • MCP-1 levels (protein and mRNA) increased significantly in response to maleate-induced kidney injury compared to NGAL.
  • Both endotoxemia and ureteral obstruction elevated NGAL and MCP-1 gene expression.
  • Uremia alone induced NGAL but not MCP-1, suggesting MCP-1's specificity for AKI.
  • Urinary MCP-1 concentrations were non-overlapping between patients with and without AKI.
  • Elevated urinary MCP-1 mRNA and H3K4m3 at the MCP-1 gene indicated gene activation in patients with renal injury.

Conclusions:

  • MCP-1 demonstrates potential as a specific biomarker for acute kidney injury.
  • Urinary histone modification analysis offers mechanistic insights into kidney disease.
  • These findings support MCP-1 as a promising biomarker for AKI diagnosis and management.

More Related Videos

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

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...
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 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 VI: Nursing Management01:22

Acute Kidney Injury VI: Nursing Management

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...
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...