Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of imaging is to establish the cause of systemic hypertension, the main focus being the kidneys. All children require a Doppler ultrasound examination followed by a radioisotope study, usually 99mTc-DMSA. This combination will resolve most clinical situations. There is no role for the intravenous urogram in the majority of children. Arteriography and renal vein renin sampling are reserved for a small proportion of children. Imaging should always start with the least invasive procedure with the lowest radiation burden and high radiation techniques reserved for selected cases. The use of ACE inhibition may allow the diagnosis of renovascular disease in paediatrics noninvasively.
 ...
PMID:Imaging in systemic hypertension in paediatrics. 806 86

Renovascular disease is an important cause of hypertension in children because it is potentially treatable by surgical or angioplasty techniques. The aim of this study was to assess the accuracy of radio-isotopes (DMSA, DTPA and MAG3) combined with the angiotensin converting enzyme inhibitor, captopril, in detecting children with renovascular hypertension. We retrospectively reviewed the ultrasound and pre- and post-captopril radionuclide studies (either DMSA and/or DPTA and/or MAG3) of children with sustained hypertension investigated at our institution. Renal angiography was used as the 'reference technique'. Thirty-nine children, over a period of 10 years, were evaluated: 17 (44%) children had renovascular disease that involved the proximal three divisions of the renal arteries, some of which were amenable to treatment. The overall sensitivity, specificity, positive predictive value and negative predictive value for detecting such renovascular disease, as assessed by changes between pre- and post-captopril radio-isotope studies, were disappointing at 59%, 68%, 59% and 68%, respectively. When considering only abnormalities in post-captopril studies, these indices were 82%, 41%, 52% and 75%, respectively. Three children with potentially treatable renovascular disease were not identified on the captopril studies. We conclude that renal angiography should remain the 'reference technique' in identifying children suspected of renovascular hypertension.
 ...
PMID:The investigation of renovascular hypertension in children: the accuracy of radio-isotopes in detecting renovascular disease. 942 1

Renal scarring with and without vesicoureteral reflux (VUR) has been now recognized as an important cause of paediatric hypertension for many years [1-5]. However, its pathogenesis has still remained uncleared. The widespread concept implicated the activation of renin-angiotensin system finding a powerfull support in higher peripheral plasma renin activity (PRA) in children with reflux nephropathy than in controls [6, 7] and in beneficial antihypertensive effects of ACE inhibitors. The latter, in form of captopril, has also been used in captopril test and in renal scintigraphy and isotope renography following the administration of captopril to provide evidence for renin dependent hypertension [8, 9]. Published studies of captopril test have centred on the identification of renovascular as opposed to essential hypertension [10-18, 20-22]. The aim of our study was to assess the usefulness of captopril test in differentiation between hypertensive children with renal scarring from those with essential hypertension. We studied blood pressure (BP) and PRA responses to a single dose of captopril in two groups of hypertensive children. Group A consisted of 29 patients, 14 boys and 15 girls, who had renal scaring as demonstrated by renal 99mTc dimercaptosuccinid acid scan (99m Tc DMSA) and/or intravenous pyelography. Group B included 19 patients, 19 boys and 10 girls who had arterial hypertension, while clinical examination excluded renal and other definable causes of BP elevation, and they were therefore considered to have essential hypertension. At the time of the study all patients had normal glomerular filtration rate and were not salt depleted. They did not receive any antihypertensive medication for at least two weeks. The test was performed in the morning in fasting sitting patients. At the start of the test a small vein in the hand or forearm was cannulated to permit blood sampling. BP was measured 10, 20, and 30 minutes before captopril administration to get baseline BP (mean of these three measurements) and to allow the children to become accustomed to the test procedure. A single oral dose of captopril 0.64 +/- 0.04 mg/kg body weight was given to patients from group A and almost the same dose of captopril, 0.63 +/- 0.05 mg/kg body weight, to patients from group B. The patients remained sitting and BP was measured every 15 minutes during an hour. Blood for PRA was drown in the sitting position (17 patients from group A and 16 patients from group B) before and one hour after the dose of captopril. Samples of blood for basal PRA were collected from 16 patients from group A and in 14 patients from in B in lying position after waking up in the morning. PRA was measured by radioimmunoassay using a commercially available kit, SB-REN 2, from CIS Bio International. According to the criteria of Muller et al. [10] the captopril test was positive if the post-captopril PRA (ng/ml/h) was greater than or equal to 12 with an increase of greater than or equal to 10 and relative increase of greater than or equal to 15% (400% if initial PRA was < 3). The results of our study are presented in Tables 1 and 2 and in Graphs 1 and 2. The age of patients, doses of captopril, initial BP and PRA before the use of captopril did not much differ between studied groups. Fall of BP and PRA increase were highly significant (p < 0.001) both in group A and group B. However, the hypotensive reaction of diastolic BP and MAP were more pronounced in group A (14.45 +/- 1.67% and 15.81 +/- 1.62%) than in group B (6.95 +/- 2.21% and 8.96 +/- 1.75%; p < 0.01), but there were no significant differences in PRA and systolic BP changes and positive results of captopril test between the studied groups. Hypotensive responses of diastolic BP and MAP greater than 10% of initial values were found to be more frequent in group A (79.32% and 79.31%) than in group B (26.61% and 31.57 degrees %; p < 0.001 and p < 0.01). Diastolic BP and MAP were directly related to the dose of cap
 ...
PMID:[The captopril test--an aid in the detection of scarring nephropathy as a cause of arterial hypertension in children]. 1064 99

The pathogenesis of renal scarring after acute pyelonephritis (APN) in children is multifactorial. In addition to well-known risk factors (young age, high grade of vesicoureteral reflux, P-fimbriated Escherichia coli, and treatment delay), a role for genetic predisposition has been suggested. Since the ACE gene deletion polymorphism is a known risk factor for progressive glomerulosclerosis in chronic renal diseases, we have investigated the relationship between the ACE genotypes and the development of renal scarring after APN. Fifty-nine children (43 males and 16 females) with APN diagnosed by urine culture and technetium-99m-dimercaptosuccinic acid ((99)Tc-DMSA) renal scan were studied. ACE genotypes were determined as II, ID, and DD using the polymerase chain reaction technique. A follow-up (99)Tc-DMSA renal scan was performed to evaluate the development of renal scars 3-6 months after treatment. The distribution of ACE genotypes and the allele frequencies were compared in the renal scar-positive ( n=39) and -negative group ( n=20). ACE genotype frequency after stratification by risk factors was also evaluated. The distribution of ACE genotypes did not differ between the renal scar-positive (II 25.9%, ID 35.9%, DD 28.2%) and -negative group (II 35.0%, ID 45.0%, DD 20.0%), before and after stratification by each risk factor. ACE gene deletion polymorphism did not affect the development of renal scar as an independent variable in children with APN.
 ...
PMID:ACE gene polymorphism and renal scar in children with acute pyelonephritis. 1217 60

Reflux nephropathy is an acquired focal renal scarring due to the combination of vesicoureteral (VUR) and intrarenal reflux (IRR) associated with urinary tract infections (IUT) and/or permanently high intravesical pressure. Up to 30-60% of children with VUR and a history of symptomatic IUT have renal scarring at the time of their initial studies. The onset of renal scarring usually occurs early in life, usually before age five years and most frequently before three years of age. Girls are at greater risk for developing reflux nephropathy, because of increased incidence of IUT. Reflux nephropathy is different from a diffuse congenital renal scarring (hypo-dysplasia), which is usually discovered antenatally or during infancy in boys with severe VUR. Without serial follow-up (ultrasonography, intravenous pyelourography, 99mTc-DMSA scan) from birth, it is not always possible to differentiate congenital renal scarring from reflux nephropathy. In contrast to reflux nephropathy, congenital renal scarring cannot be prevented. 99mTc-DMSA renal scintigraphy is the gold standard technique (sensitivity 92%, specificity 98%) for the diagnosis of reflux nephropathy, but ultrasound is a good modality to monitor kidney growth over time. Reflux nephropathy and hypodysplasia are the main causes of chronic renal failure and arterial hypertension in children and adolescents in our country. The long-term follow-up of children with reflux nephropathy is mandatory, since its complications may take 10 to 20 years to develop. Uncontrollable arterial hypertension and proteinuria are the predictors of poor prognosis. The selective use of angiotensin converting enzyme inhibitors and/or angiotensin II receptor blockers is the efficient antihypertensive therapy, which also modify intrarenal haemodynamics and can preserve renal function.
 ...
PMID:[Vesicoureteral reflux and renal scarring]. 1836 11