Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin I converting enzyme (ACE) activity was measured in serum, urine, and tissues of rats with acute renal failure (ARF) induced by glycerol. Glycerol-injected rats were subdivided in three groups according to the urinary volume: oliguric, nonoliguric, and polyuric. The damage to the proximal tubule was evident by (a) the histological analysis at light and electron microscopy level, (b) the augmented urinary excretion of the enzymes dipeptidyl aminopeptidase IV and N-acetyl-beta-D-glucosaminidase, and (c) the low molecular weight proteinuria pattern. On the other hand, the appearance of the glomeruli at the ultrastructural level was normal. These data suggest that the increased urinary excretion of enzymes and proteins in these rats is a consequence of the tubular injury. ARF was markedly higher in the oliguric rats. Urine ACE activity increased in the rats of the three groups, but statistical significance was reached only in the oliguric rats. Serum ACE activity increased in the oliguric rats and tissue ACE activity did not change. It is concluded that the high urinary ACE in glycerol-treated rats is associated with the damage to the kidney tubules. These data support the contention that urinary ACE may be another marker of injury to the proximal tubule.
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PMID:Angiotensin I converting enzyme in glycerol-induced acute renal failure in rats. 756 9

Angiotensin I converting enzyme (ACE) was measured in urine, serum, and tissues from rats with acute renal failure (ARF) induced by a single subcutaneous injection (15 mg/kg BW) of uranyl nitrate (UN). Urine was collected daily until day 5, when rats were sacrificed by decapitation for the obtention of blood serum and tissues. Other groups of rats were sacrificed on days 1 and 2. These rats showed proteinuria and polyuria. The damage to the kidney proximal tubule was shown by (a) histological analysis at light and electron microscopy levels on days 1, 2, and 5, (b) the increase in urinary excretion of dipeptidyl aminopeptidase IV and N-acetyl-beta-D-glucosaminidase on days 1-5, and (c) the low molecular weight proteinuria pattern on day 1. In addition, the histological analysis at the ultrastructural level showed normal glomeruli appearance on days 1 and 2, but structural alterations on day 5. These data suggest that the increased urinary excretion of enzymes and proteins is a consequence of the tubular injury on days 1 and 2, and of tubular and glomerular injury on day 5. ACE activity increased in urine on days 1-5 and in serum on day 5. Tissue ACE activity increased in lung, small intestine, and adrenal glands; and remained unchanged in testis, aorta, brain, kidney, heart, and liver. Our data suggest that: (a) the increase in serum ACE may be secondary to the changes in tissue ACE activity, and (b) the urine ACE increase may be due to the kidney proximal tubule damage. This work supports the contention that an increase in urine ACE may be an indicator of injury to the proximal tubule.
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PMID:Angiotensin I converting enzyme activity in uranyl nitrate induced acute renal failure in rats. 756 10

Angiotensin I converting enzyme inhibition (ACEi) has been shown to lower urinary protein excretion in human renal disease. The mechanism of this antiproteinuric effect is hypothesized to be mediated by changes in renal hemodynamics. However, clinical studies suggest that the effect on renal hemodynamics is fully established immediately after the start of treatment, whereas others show the antiproteinuric effect to reach maximum only after several weeks. To clarify this issue we studied the course of renal hemodynamics, blood pressure and proteinuria during 28 days of ACEi (enalapril 10 mg oid) in nine patients with proteinuria due to non-diabetic renal disease. The effect of ACEi on blood pressure and renal hemodynamics was already maximal within few hours after start of treatment, and remained stable thereafter: MAP was lowered with 8.6 +/- 1.9%, 10.6 +/- 2.1%, 12.8 +/- 2.3% and 12.9 +/- 2.5%, while FF fell 23.0 +/- 2.0%, 17.0 +/- 2.6%, 16.8 +/- 2.8% and 15.9 +/- 4.0% on days 1, 7, 14 and 28 of ACEi, respectively. However, the antiproteinuric effect only gradually reached its maximum on day 28. Urinary protein excretion decreased with 10.9 +/- 6.1%, 32.7 +/- 6.2%, 46.3 +/- 2.5% and 54.0 +/- 2.5% on days 1, 7, 14 and 28 of ACEi, respectively. After drug withdrawal all parameters returned towards baseline. We conclude that a dissociation occurs in the course of the ACEi induced effects on hemodynamics and urinary protein excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dissociation between the course of the hemodynamic and antiproteinuric effects of angiotensin I converting enzyme inhibition. 823 Oct 31