Related Experiment Video

Updated: Aug 13, 2026

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
08:50

5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

Published on: July 3, 2013

[Long-term effect of angiotensin-converting inhibitors in children with proteinuria]

J A Camacho Díaz1, A Giménez Llort, L García García

  • 1Sección Nefrología. Unidad Integrada Hospital Clínic-Hospital Sant Joan de Déu. Universidad de Barcelona. jcamacho@hsjdbcn.org

Anales Espanoles De Pediatria
|October 26, 2001
PubMed

Insights

Low-dose angiotensin-converting enzyme (ACE) inhibitors effectively reduced proteinuria in children with chronic kidney disease without adverse effects. This offers a safe, long-term treatment option for pediatric nephropathy.

Area of Science:

  • Pediatric Nephrology
  • Pharmacology
  • Renal Medicine

Context:

  • Prolonged proteinuria is a significant risk factor for progressive renal damage.
  • Angiotensin-converting enzyme (ACE) inhibitors are established treatments for proteinuria in adults.
  • Limited data exists on the long-term efficacy and safety of ACE inhibitors in pediatric chronic nephropathies.

Purpose:

  • To evaluate the efficacy and safety of low-dose ACE inhibitors (captopril and enalapril) in children with proteinuria due to chronic glomerular nephropathy.
  • To assess the impact of prolonged ACE inhibitor treatment on proteinuria levels, glomerular filtration rate, and arterial pressure in pediatric patients.

Summary:

  • Nine children with various chronic glomerular nephropathies received low-dose ACE inhibitors for a mean of 26.6 months.
  • Significant reductions in proteinuria were observed within 6 months and sustained throughout the treatment period.
  • No adverse reactions, significant changes in glomerular filtration rate, or arterial pressure were noted.

Impact:

  • Low-dose ACE inhibitors represent a safe and effective therapeutic alternative for managing proteinuria in children with chronic nephropathies.
  • Prolonged use of ACE inhibitors in pediatric patients with nephropathy is well-tolerated and avoids adverse effects associated with other treatments.
  • This study supports the use of ACE inhibitors as a long-term strategy to mitigate renal damage in children with persistent proteinuria.
Abstract

More Related Videos

Induction of Nephrotic Syndrome in Mice by Retrobulbar Injection of Doxorubicin and Prevention of Volume Retention by Sustained Release Aprotinin07:38

Induction of Nephrotic Syndrome in Mice by Retrobulbar Injection of Doxorubicin and Prevention of Volume Retention by Sustained Release Aprotinin

Published on: May 6, 2018

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells09:40

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells

Published on: June 20, 2018

Related Concept Videos

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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 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...