Biomedical subjects
Publications and source records attributed to Ferenc Papp.
We performed 43 open partial nephrectomies with different indications between 1996 and 2004, most of them (29) for renal cancer. We used different types of biocompatible materials for haemostasis. We describe our own recommendations and what is described in literature.
The effects of levamisole treatment on long-term outcome were evaluated in a retrospective study of frequently-relapsing (FRNS, n=15), steroid-dependent (SDNS, n=13), and steroid-resistant (SRNS, n=6) nephrotic syndrome in 34 children (21 boys, 13 girls, mean age 5.0+/-3.4 years) during a 60-month follow-up period. The definition of frequent relapses was > or = 4 relapses per year. The current relapse was treated with prednisolone 60 mg/m2 per day for 4 weeks, then with 40 mg/m2 every other day for 4 weeks, after which the dose was tapered by 10 mg weekly. From the beginning of the 5th week, levamisole was introduced at a dose of 2 mg/kg per day. The duration of levamisole treatment was 17+/-7 months. Before starting levamisole treatment the mean level of proteinuria was 2.17+/-1.34 g/day and the relapse rate was 4.41/year. By the end of levamisole therapy, proteinuria had fallen to 0.142+/-0.211 g/day and the relapse rate to 0.41/year. No relapse occurred in 23 of the 34 patients during levamisole treatment. In the 24-month follow-up period after the discontinuation of levamisole, 28 children remained in total remission, while 6 had relapses. The cumulative steroid dose before levamisole therapy was 7,564.4+/-3,497.1 mg/year and following the introduction of levamisole 1,472.9+/-1,729.9 mg/year (P<0.0001). We observed reversible neutropenia in 5 patients, but no other side effects were seen. Our findings suggest that in FRNS and SDNS levamisole significantly reduces both the relapse rate and the cumulative steroid dose; therefore, it could be recommended for these patients. In SRNS patients it has also some benefit because proteinuria and the cumulative steroid dose could be reduced significantly.
UNLABELLED: A group of 35 patients (median age 15.5 years, range 8-17 years) with juvenile essential hypertension, 15 with body mass index (BMI kg/m(2)) <25 and 20 with BMI >25, as well as 35 age and sex matched controls (BMI <25 n=20; BMI >25 n=15) were investigated to study the role of hypertension and obesity, separately and in combination, on in vitro platelet aggregation, blood and plasma viscosity, plasma lipid concentrations and lipid peroxidation as well as nitric oxide (NO) production. Obese children (hypertensive and controls) had significantly higher concentrations of total cholesterol and triglycerides. The levels of high density lipoprotein (HDL)-cholesterol were lower in obese hypertensive children than their non-obese counterparts. There was a significant increase in platelet aggregation and a decrease in NO levels in hypertensive patients (obese and non-obese) reflecting a significant negative correlation (r=-0.553 and -0.530, n=35; P<0.01, respectively). However, an increased tendency to aggregation was also evident in obese normotensive patients. A significant positive correlation was observed between the platelet aggregation and BMI (r=0.501, n=35; P<0.01). Plasma free thiols were decreased in hypertensive children independent of their BMI. An increased lipid peroxidation and higher blood and plasma viscosity were found only in obese patients with hypertension. Multivariate analysis revealed significant interactions in the effects of obesity and hypertension on platelet aggregation and thiol oxidation. CONCLUSION: in obese children an increased platelet aggregation and oxidative insult contribute to the development of hypertension and to the promotion of vascular damage.
OBJECTIVE: Oxidative stress, an antioxidant/pro-oxidant imbalance, in patients with juvenile essential hypertension was measured via several biochemical parameters. As the blood pressure is associated with the body mass index (BMI), results were compared with those on BMI-matched controls. DESIGN AND SETTING: A prospective observational study at a university teaching hospital. PATIENTS: Children and adolescents with essential hypertension (mean standard deviation: age 14.4 +/- 3.1 years, BMI 25.0 +/- 6.9 kg/m(2), n = 52) before any treatment, and controls with a similar BMI distribution (age 14.3 +/- 4.3 years, BMI 24.4 +/- 6.6 kg/m(2), n = 48). METHODS: Measurements were made of the plasma levels of (1) nitrites + nitrates, an indirect measure of available nitric oxide; (2) lipid peroxidation end-products, as malondialdehydes and free thiols; and (3) the redox status of the red blood cell glutathione, as a new oxidative stress parameter. RESULTS: There were decreased plasma levels of nitrates and increased levels of lipid peroxidation end-products in the hypertensive patients, resulting in a consistent increase in the plasma lipid peroxidation/nitric oxide ratio as compared with the controls with the same BMI (P <0.01). This ratio additionally correlated directly with both the systolic and diastolic blood pressures for the overall patient population (P <0.001). A significant glutathione depletion in the red blood cells resulted in an elevated ratio of oxidized/reduced forms with a reduced antioxidant protective capacity in the hypertensive patients versus the BMI-matched controls (P <0.001). CONCLUSIONS: The presence of systemic oxidative stress was proven in hypertensive children and adolescents, irrespective of their BMI.
The M235T polymorphism of the angiotensinogen (ANG) gene, the I/D polymorphism of the angiotensin converting enzyme (ACE) gene, and the A1166C polymorphism of the angiotensin II type 1 receptor (AT1R) gene were identified in 70 patients with end-stage renal disease [20 pediatric ESRD, aged 14.9+/-3.1, years blood pressure (BP) 139+/-14/91+/-13 mmHg, 50 adult ESRD, aged 48.7+/-18.7 years, BP 149.1+/-24/96.9+/-12 mmHg], 35 with juvenile essential hypertension (JEHT, aged 14.4+/-2.7 years, 24-h mean BP 135.37+/-7.37/72.4+/-7.68 mmHg), 130 adult healthy normotensive controls (aged 34.9+/-8.1 years, BP 117.8+/-8.7/78.7+/-8.5 mmHg), and 20 pediatric controls (aged 13.2+/-1.2 years, BP 109+/-6.5/71+/-5.9 mmHg). The ACE gene polymorphism was determined by polymerase chain reaction and the ANG and AT1R gene polymorphisms by single-step LightCycler technology. The ACE gene distribution of the Hungarian controls did not differ from the results of the other Caucasian populations. In JEHT and pediatric ESRD patients, the MT genotype of ANG was more frequent than in controls (JEHT 80%, pediatric ESRD 74% versus controls 50%, P<0.02). The DD genotype of ACE was over-represented in pediatric ESRD compared with controls (ESRD 45% versus controls 22%, P<0.05). There was a non-significant increase in the CC genotype frequency of AT1R in adult patients with ESRD compared with controls. In conclusion, there was an increased frequency of the ACE DD genotype in pediatric ESRD, which could be a genetic risk factor for the development of ESRD. Furthermore, there was a significant increase in MT genotype frequency of ANG M235T polymorphism in pediatric ESRD and JEHT. The role of AT1R gene polymorphism needs further investigation.
The objective of this study was to investigate whether mutations of the renin-angiotensin system genes are involved in primary vesicoureteric reflux (VUR) and VUR-associated renal scarring. The M235T polymorphism of the angiotensinogen ( ATG) gene, the I/D polymorphism of the angiotensin converting enzyme ( ACE) gene, and the A1166C polymorphism of the angiotensin II type 1 receptor ( AT1) gene were identified in 77 patients with primary VUR (aged 6.9+/-3.2 years, mean+/-SD) and 80 healthy controls (aged 33+/-7 years). Thirty-eight of the 77 VUR patients had low-grade VUR (grade I-III) and 39 had high-grade VUR (grade IV and V). Renal scarring was found in 43 VUR patients, while 34 patients had normal kidneys on dimercaptosuccinic acid scan. The ACE gene polymorphism was determined by polymerase chain reaction and the ATG and AT1 gene polymorphisms were determined by single-step LightCycler technology. We found significant over-representation of the DD genotype in patients with renal scarring (44 %) compared with normal controls (23%, P<0.05) and patients with no scar formation (21%, P<0.05). Significantly higher D and significantly lower I allele frequencies were present in VUR patients with scarred kidneys (D allele 0.64 and I allele 0.36) compared with controls (D allele 0.53 and I allele 0.47, P<0.05) and patients with unscarred kidneys (D allele 0.4 and I allele 0.6, P<0.05). No differences in the ATG and AT1 genotype distributions and allele frequencies were observed in VUR patients compared with the normal population. The DD genotype and D allele of ACE may be a genetic susceptibility factor contributing to scar formation in VUR. We detected no linkage of genetic polymorphisms of ATG and AT1 to VUR and VUR-associated renal scarring.