Related Experiment Video

Updated: Aug 29, 2026

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
07:52

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Published on: November 7, 2017

Homocysteine and left ventricular hypertrophy in children with chronic renal failure

Hakan M Poyrazoğlu1, Ruhan Düşünsel, Figen Narin

  • 1Department of Pediatric Nephrology, Erciyes University Medical Faculty, 38039 Kayseri, Turkey. drpoyrazoglu@yahoo.com

Pediatric Nephrology (Berlin, Germany)
|December 6, 2003
PubMed

Insights

In children with chronic renal failure (CRF), elevated plasma homocysteine and left ventricular hypertrophy were observed. However, homocysteine did not directly correlate with left ventricular mass index in these patients.

Area of Science:

  • Nephrology
  • Cardiology
  • Pediatrics

Background:

  • Hyperhomocysteinemia is a known cardiovascular disease risk factor in adults with chronic renal failure (CRF).
  • Limited data exists on the link between plasma homocysteine and left ventricular hypertrophy (LVH) in pediatric CRF patients.

Purpose of the Study:

  • To assess plasma homocysteine levels and risk factors for LVH in children with CRF.
  • To investigate the relationship between plasma homocysteine concentration and left ventricular mass index (LVMI) in pediatric CRF.

Main Methods:

  • Measured plasma homocysteine using high-performance liquid chromatography.
  • Calculated LVMI via echocardiography in 27 children with CRF and 16 controls.

Main Results:

  • CRF patients, particularly those with end-stage renal disease, showed higher mean LVMI and plasma homocysteine than controls (P<0.05).
  • No correlation was found between LVMI and plasma homocysteine.
  • Positive correlations observed between plasma homocysteine and serum creatinine.
  • LVMI correlated positively with creatinine and blood pressure, and negatively with hemoglobin.

Conclusions:

  • Homocysteine does not appear to directly impact left ventricular structure in pediatric CRF.
  • Left ventricular hypertrophy in these children is likely end-organ damage linked to hypertension, anemia, and CRF.
  • Further prospective studies are needed to clarify the interplay between plasma homocysteine and left ventricular structure in pediatric CRF.

Related Concept Videos

Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers01:19

Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers

Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Chronic Kidney Disease I: Introduction01:25

Chronic Kidney Disease I: Introduction

Chronic Kidney Disease (CKD) arises when the kidneys progressively lose their ability to function, ultimately leading to end-stage renal disease. At this advanced stage, the kidneys can no longer filter waste or maintain essential body functions, requiring renal replacement therapy (RRT) through dialysis or a kidney transplant for survival.Early-stage chronic kidney disease and detection challengesIn CKD's early stages, symptoms often remain absent because healthy nephrons compensate for...
Renal Failure: Dose Adjustments01:11

Renal Failure: Dose Adjustments

In patients with renal impairment, drugs undergo significant changes in their pharmacokinetics, which require dosage adjustments to ensure safe and effective therapy.
Reduced renal clearance and elimination rate are common outcomes of renal impairment. These alterations lead to a prolonged elimination half-life and an altered apparent volume of distribution for drugs. As a result, dosage adjustments are typically necessary to maintain optimal drug levels in the body.
However, dosage adjustments...
Mitral Regurgitation I: Introduction01:20

Mitral Regurgitation I: Introduction

Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...