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

Background

Human tissue kallikrein (hK1) is a key enzyme in the kallikrein–kinin system(KKS). hK1-specific amidase activity is reduced in urine samples from hypertensiveand heart failure (HF) patients. The pathophysiologic role of hK1 in coronaryartery disease (CAD) remains unclear.

Objective

To evaluate hK1-specific amidase activity in the urine of CAD patients

Methods

Sixty-five individuals (18–75 years) who underwent cardiac catheterism (CATH) wereincluded. Random midstream urine samples were collected immediately before CATH.Patients were classified in two groups according to the presence of coronarylesions: CAD (43 patients) and non-CAD (22 patients). hK1 amidase activity wasestimated using the chromogenic substrate D-Val-Leu-Arg-Nan. Creatinine wasdetermined using Jaffé’s method. Urinary hK1-specific amidase activity wasexpressed as µM/(min · mg creatinine) to correct for differencesin urine flow rates.

Results

Urinary hK1-specific amidase activity levels were similar between CAD [0.146µM/(min ·mg creatinine)] and non-CAD [0.189µM/(min . mg creatinine)] patients (p = 0.803) and remainedsimilar to values previously reported for hypertensive patients [0.210µM/(min . mg creatinine)] and HF patients [0.104µM/(min . mg creatinine)]. CAD severity and hypertension werenot observed to significantly affect urinary hK1-specific amidase activity.

Conclusion

CAD patients had low levels of urinary hK1-specific amidase activity, suggestingthat renal KKS activity may be reduced in patients with this disease.