Tips for the use of antihypertensive drugs: DELTAREPROSI.
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Biomedical subjects
Publications and source records attributed to Mario G Bianchetti.
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PURPOSE: We evaluated the role of family history, infrequent voiding, poor fluid intake, functional stool retention and inadequate anogenital hygiene or toilet habits in girls with recurrent urinary tract infections. MATERIALS AND METHODS: The possible occurrence of these risk factors was assessed in 90 Swiss girls with recurrent urinary tract infections and in a control group of 45 girls. RESULTS: Family history was positive in 42% of patients and in 11% of controls (p <0.001). Behavioral abnormalities were also more frequently noted in girls with recurrent urinary tract infections than in the control group (81% vs 56%, p <0.01). There were 137 abnormalities in 73 girls with recurrent urinary tract infections and 30 abnormalities in 25 controls. Two or more abnormalities each, that is 2 in 32 girls and 3 in 16, were noted in 48 girls with recurrent urinary tract infections and in 5 control girls. No controls presented with more than 2 abnormalities. Infrequent voiding (54% vs 24%, p <0.001), poor fluid intake (53% vs 16%, p <0.001) and functional stool retention (30% vs 13%, p <0.05) were more frequently disclosed in girls with recurrent urinary tract infections than in control girls. In contrast, the frequency of inadequate stool hygiene or toilet habits was similar in patients and controls (14% and 13%, respectively). CONCLUSIONS: The evaluation of girls with recurrent urinary tract infections should focus on identifying behavioral aspects, including infrequent voiding, poor fluid intake and functional stool retention.
Long-lasting recovery of renal function of the native kidneys after prolonged renal replacement therapy is rare. An 8-year-old girl and a 3-year-old boy had suffered from acute atypical and diarrhea-associated hemolytic uremic syndrome (HUS), respectively, with subsequent apparent end-stage renal failure. Both recovered renal function after long-lasting anuria and dialysis of 8 and 16 months, respectively. After prolonged follow-up, i.e., 7 and 5 years after cessation of dialysis, they attained normal or slightly reduced renal function (plasma creatinine 84 and 90 micro mol/l, respectively). In addition, growth and cognitive development were normal. We conclude that caution is appropriate before offering early renal transplantation to pediatric patients with presumed end-stage kidney disease secondary to HUS.
A 12-month-old boy developed a mild hemolytic uremic syndrome with no acute diarrheal prodrome. The typical clinical, hematological, and serological features of infectious mononucleosis were also noted. The clinical course of both hemolytic uremic syndrome and infectious mononucleosis was uneventful. A review of the literature disclosed that hemolytic uremic syndrome has been noted in two adolescents with infectious mononucleosis.
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BACKGROUND: Efforts are now routinely made for early detection of vesicoureteric reflux after urinary tract infections in order to limit secondary renal damage. METHODS: The age at diagnosis of reflux after urinary tract infections was analysed in 162 Swiss patients (46 boys and 116 girls) referred by primary care physicians to the Division of Paediatric Nephrology, University of Bern, Switzerland between 1978 and 1999. The figures noted in Switzerland were also compared with those noted in 102 Australian patients (35 boys and 67 girls) reported by Lenaghan in 1976. RESULTS: In Switzerland the median age at diagnosis was 23 months in 74 subjects diagnosed between 1978 and 1988 and 10 months in 88 subjects diagnosed between 1989 and 1999. The difference was statistically significant in girls but not in boys. In Australia the median age at diagnosis was 15 months for boys and 78 months for girls; in Switzerland, the corresponding figures were 12 and 29 months (between 1978 and 1988), respectively 5 and 14 months (between 1989 and 1999). The difference between Australia and Switzerland was statistically significant in girls but not in boys. CONCLUSIONS: In Switzerland vesicoureteric reflux is now detected earlier than in the past. This trend is more marked in girls than in boys but the detection of reflux is still earlier in boys than in girls.
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Regulation of magnesium balance is achieved by a steady-state mechanism in which intake and output are maintained at an equal level. Dietary magnesium intake, total and ionized plasma magnesium levels, and urinary magnesium were assessed in 46 renal transplant recipients treated with cyclosporine, nine transplant recipients who had never been on cyclosporine, and 31 healthy volunteers. Dietary magnesium intake [13.5 (11.0-15.1) mmol/day vs 13.0 (11.1-16.0) mmol/day and 13.7 (11.4-16.7) mmol/day, respectively; median and interquartile range] and urinary magnesium excretion [4.31 (3.57-5.89) vs 4.39 (3.56-6.02) and 5.01 (3.73-6.01) mmol/day, respectively] were similar in renal transplant recipients treated with cyclosporine, transplant recipients who had never been on cyclosporine, and control subjects. Total [0.74 (0.70-0.78) vs 0.80 (0.74-0.84) and 0.81 (0.79-0.87) mmol/l), respectively] and ionized [0.49 (0.46-0.52) vs 0.53 (0.50-0.58) and 0.54 (0.52-0.59) mmol/l, respectively] plasma magnesium were significantly lower in renal transplant recipients on cyclosporine than in transplant recipients without cyclosporine, and healthy controls. These observations indicate a modified magnesium steady state in renal transplant recipients treated with cyclosporine.
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Potassium deficiency predisposes to cardiac arrhythmias culminating in syncope or sudden death. Because of the uncertainty related to the possible occurrence of such cardiac arrhythmias in the context of normotensive-hypokalemic tubulopathies, 19 European pediatric nephrologists with a large experience of normotensive-hypokalemic tubulopathies were asked to answer a questionnaire. The responses suggest that inherited normotensive-hypokalemic tubulopathies per se do not strongly predispose to dangerous cardiac arrhythmias. However, cardiac arrhythmias may be acutely precipitated by drugs that prolong the QT interval, by diarrhea, or vomiting, and perhaps even by physical activity. Finally, the likelihood of dangerous arrhythmias in normotensive-hypokalemic tubulopathy is currently unknown.
BACKGROUND: The dihydropyridine calcium channel blocker amlodipine and the angiotensin II antagonist irbesartan effectively reduce blood pressure in hypertensive children. METHODS: Eligible for the open-label, randomized study were nephropathic children between 6.0 and 18 years of age with plasma creatinine <177 micromol/L, overt proteinuria, untreated arterial hypertension (systolic, 5 to 30 mm Hg; and diastolic, 1 to 15 mm Hg;>95th centile) and stable immunosuppressive treatment. The initial dose of amlodipine was 5 mg (body weight, 20 to 40 kg) and 10 mg (body weight,>40 kg), respectively, that of irbesartan, which was 75 mg (body weight, 20 to 40 kg) and 150 mg (body weight,>40 kg), respectively. The dosage was doubled if necessary. RESULTS: A total of 26 children aged 6.1 to 17 years were allocated to receive either amlodipine (N = 13) or irbesartan (N = 13) for 16 weeks. Severe edema and headache occurred in two patients on amlodipine who withdrew from the study. No adverse experiences were noted in patients given irbesartan. Amlodipine [by 12 (10 to 14)/7 (5 to 10) mm Hg; median and interquartile range, respectively] and irbesartan [by 13 (9 to 16)/9 (7 to 11) mm Hg, respectively] reduced blood pressure (P < 0.01) in a similar fashion. Heart rate, plasma sodium, and creatinine did not change. Irbesartan slightly increased plasma potassium [by 0.1 (0.0 to 0.2) mmol/L; P < 0.05]. Plasma albumin and the urinary albumin/creatinine ratio were similar before and with amlodipine. On the contrary, irbesartan increased plasma albumin [by 4 (3 to 5) g/L; P < 0.03] and decreased the urinary albumin/creatinine ratio [by 242 (68 to 312) mg/mmol; P < 0.03]. CONCLUSION: The study demonstrates that in children the effect of angiotensin II antagonists on proteinuria is better than that of dihydropyridine calcium channel blockers.
BACKGROUND: Since good control of arterial hypertension is of paramount importance, the present study was carried out to evaluate blood pressure control in pediatric patients with hypertension receiving regular medical care. STUDY DESIGN: The charts of 80 hypertensive children receiving medical care were reviewed. Their antihypertensive medication had been stable during three or more separate clinic visits and during 3 or more months. Patients with office hypertension were excluded. RESULTS: Blood pressure values higher than the corresponding 95th centiles were noted in 20 of the 80 patients. Hypertension was systolic in seven, diastolic in four and both systolic and diastolic in nine patients. The number of prescribed antihypertensive drugs and the number of doses/day of prescribed antihypertensive drugs was similar in patients with good and in those with poor blood pressure control. Plasma creatinine was higher in patients with poor than in those with good blood pressure control. CONCLUSIONS: The present survey indicates that the goal of antihypertensive medication is not achieved in a noticeable number of pediatric patients with treated hypertension.
Renal ultrasound scan, circulating creatinine and calcium, and the urinary calcium excretion rate were investigated in 57 patients with clinically and genetically typical Williams-Beuren syndrome (25 female and 32 male subjects, aged from 1.0 year to 23 years, median 8.5 years) on regular follow up at our institution. Twenty-three unilateral abnormalities were detected in 20 patients: pelvic dilatation ( n=6), renal hypoplasia ( n=5), isolated renal cyst ( n=3), kidney surface irregularity ( n=3), kidney duplication ( n=2), renal agenesis ( n=1), megaureter ( n=1), pelvic kidney dystopia ( n=1), and renal stone ( n=1). Both infantile hypercalcemia and nephrocalcinosis was absent in the 57 patients. Mild hypercalcemia was noted in 1 and mild hypercalciuria in 2 patients after the 1st year of life. In conclusion, the study indicates the frequent occurrence of intrinsic renal tract abnormalities detected by ultrasonography in Williams-Beuren syndrome. However, the study does not confirm the importance given in the past to the occurrence of hypercalcemia and hypercalciuria.
BACKGROUND: Studies in adults with chronic kidney diseases demonstrate that the orally available angiotensin II antagonist irbesartan reduces arterial pressure and pathological proteinuria, mostly with an excellent tolerability profile. Little information is available on irbesartan in childhood. METHODS: A total of 44 pediatric outpatients with chronic kidney disease (27 male and 17, aged 3.7 to 18 years, median 10 years) were given irbesartan once a day during 18 weeks for arterial hypertension (N = 23), proteinuria (N = 8), or both (N = 13). RESULTS: In patients with hypertension, the use of irbesartan 4.1 (3.1-5.3) mg/kg body weight daily (median and interquartile range) was associated with a decrease (P <.005) in arterial pressure by 17 (13-22)/10 (7-12) mm Hg. In patients with overt proteinuria the urinary protein excretion decreased (P <.01) during treatment with irbesartan (2.9 [2.0-4.8] mg/kg body weight) by 52 (0-75) mg/[m(2) x h]), whereas plasma albumin increased (P <.05) by 4 (1-5) g/L. The frequency of abdominal pain, constipation, cough, diarrhea, dizziness, edema, fatigue, headache, insomnia, myalgia, orthostasis, and rash was similar before and with irbesartan. Plasma sodium slightly decreased, whereas plasma potassium increased, with irbesartan (P <.01). CONCLUSIONS: In pediatric patients with chronic kidney diseases, irbesartan given once a day for 18 weeks significantly reduces arterial pressure and proteinuria, with an excellent tolerability and side effect profile.
BACKGROUND: Potassium and magnesium deficiency prolong the QT interval on a standard electrocardiogram and predispose the patient to dangerous cardiac arrhythmias. No information is available on QT interval in patients diagnosed with Gitelman disease. METHODS: The QT interval was assessed on lead II in 27 patients with biochemically and genetically defined Gitelman disease, who had discontinued medical treatment for at least four weeks. They included 15 female and 12 male subjects, aged 6.7 to 40 years old, median 20 years old. The corrected QT interval was calculated from the measured QT interval and heart rate using the Bazett formula. RESULTS: The corrected QT interval was normal (between 391 and 433 msec) in 16 and prolonged in the remaining 11 patients (between 444 and 504 msec). Patients with prolonged and patients with normal QT interval did not significantly differ with respect to female to male ratio, plasma potassium, plasma total magnesium, and plasma ionized calcium. Plasma sodium and chloride values were slightly but significantly lower and bicarbonate levels higher in patients with a prolonged than in those with a normal QT interval. CONCLUSIONS: The corrected QT interval is often pathologically prolonged in patients with Gitelman disease, suggesting that there is an increased risk for development of dangerous arrhythmias. Further investigations are required in patients with a prolonged QT interval to assess the true hazard of dangerous arrhythmias.