Why the study?
Does urinary excretion of angiotensin converting enzyme differ between patients with renal diseases and normal subjects?
Does urinary excretion of angiotensin converting enzyme differ between patients with renal diseases and normal subjects?
Urinary excretion of a high molecular weight form of angiotensin converting enzyme is significantly increased in patients with nephrotic syndrome and chronic glomerulonephritis, likely reflecting proximal tubular damage.
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Elevated urinary ACE may signal tubular injury in glomerular disease; hypothesis-generating for biomarker use, needs prospective validation.
We measured the activity of angiotensin converting enzyme (ED 3.4.15.1) in urine samples from normal subjects and patients with nephrotic syndrome and chronic glomerulonephritis. Urinary excretion of angiotensin converting enzyme in patients with nephrotic syndrome (1.58 +/- 0.50 (SD) units/day; n = 15) and chronic glomerulonephritis (1.01 +/- 0.45 units/day; n = 12) was significantly increased compared with normal subjects (0.38 +/- 0.10 units/day; n = 18). It was demonstrated that a high molecular weight form of the enzyme (more than 400000) was mainly excreted in urines from patients with nephrotic syndrome. After trypsin treatment, this form was altered to a low molecular weight form (290000). These two different forms of urinary angiotensin converting enzyme were compared with the enzyme purified from human kidney, and found to be identical with respect to Km values (2 mmol/l), pH optimum (pH 8.3), chloride ion dependency (0.8 mol/l), inhibitory effect of captopril (I50, 21 nmol/l), and behavior towards antiserum to human kidney angiotensin converting enzyme.
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Kato et al. (1982) studied this question.
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