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Causes of angiotensin-converting enzyme (ACE) increases and decreases
Last reviewed: 06.07.2025
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Angiotensin-converting enzyme (ACE) is a glycoprotein that is present primarily in the lungs and in small amounts in the brush border of the renal proximal tubule epithelium, the endothelium of blood vessels, and blood plasma. ACE, on the one hand, catalyzes the conversion of angiotensin I into one of the most powerful vasoconstrictors - angiotensin II, on the other hand, hydrolyzes the vasodilator bradykinin to an inactive peptide.
Medicines - ACE inhibitors - are successfully used to reduce blood pressure in patients with arterial hypertension, as well as to prevent the development of renal failure in patients with diabetes mellitus, and to improve outcomes in patients with myocardial infarction.
Reference values (norm) for the activity of angiotensin-converting enzyme (ACE) in blood serum are 8-52 IU/L.
Determination of ACE activity is used mainly for diagnostics of sarcoidosis (sometimes - for evaluation of efficiency of ACE inhibitors). In active pulmonary form of sarcoidosis, increased ACE is detected in 85-90% of patients (in inactive form - only in 11%). The more significant the increase in ACE, the greater the prevalence and activity of the process. Typical for the disease are leukopenia (in 31% of patients), anemia (in 31%), eosinophilia (in 25%), hypergammaglobulinemia (in 50%), hypercalcemia (in 17%) and hypercalciuria (in 30%).
Increased ACE activity in the blood serum is possible in acute and chronic bronchitis, pulmonary fibrosis of tuberculous etiology, occupational pneumoconiosis (in 20% of patients), rheumatoid arthritis, connective tissue diseases, cervical lymphadenitis, Gaucher disease (in 100%), liver cirrhosis (in 25%), hyperthyroidism (in 81%), chronic kidney disease, amyloidosis, type 1 diabetes mellitus (more than 24%).
Decreased ACE activity can be detected in chronic obstructive pulmonary diseases, late stages of lung cancer and tuberculosis.