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Human Tissue Kallikrein Activity in Angiographically Documented Chronic Stable Coronary Artery Disease

Estêvão Lanna Figueiredo1, Carolina Antunes Magalhães2, Karlyse Claudino Belli3

  • 1Departamento de Cardiologia, Hospital Lifecenter, Belo Horizonte, MG, Brazil.

Arquivos Brasileiros De Cardiologia
|September 10, 2015
PubMed

Insights

Coronary artery disease (CAD) patients exhibit reduced urinary human tissue kallikrein (hK1) amidase activity, indicating potential impairment in the renal kallikrein-kinin system (KKS). This finding suggests a link between hK1 levels and cardiovascular health.

Area of Science:

  • Biochemistry
  • Cardiovascular Medicine
  • Nephrology

Background:

  • Human tissue kallikrein (hK1) is a crucial enzyme in the kallikrein-kinin system (KKS).
  • Reduced urinary hK1 amidase activity is observed in patients with hypertension and heart failure (HF).
  • The role of hK1 in coronary artery disease (CAD) pathophysiology is not well understood.

Purpose of the Study:

  • To investigate and quantify urinary hK1-specific amidase activity in patients with and without CAD.
  • To explore the association between hK1 activity and the presence and severity of coronary artery disease.

Main Methods:

  • Sixty-five patients undergoing cardiac catheterism were enrolled.
  • Urine samples were collected pre-catheterization and categorized based on coronary lesion presence (CAD vs. non-CAD).
  • Urinary hK1 amidase activity was measured using a chromogenic substrate and normalized to creatinine levels.

Main Results:

  • Urinary hK1-specific amidase activity was comparable between CAD and non-CAD groups.
  • Activity levels in CAD patients were similar to those previously reported for hypertensive and HF patients.
  • Neither CAD severity nor hypertension significantly influenced urinary hK1 amidase activity.

Conclusions:

  • Patients with CAD demonstrate diminished urinary hK1-specific amidase activity.
  • This suggests a potential reduction in renal KKS activity associated with coronary artery disease.
Abstract

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