PubMed Health⌕ Search

Biomedical subjects

M G Bianchetti

Publications and source records attributed to M G Bianchetti.

At least 91 records · Page 5Linked to original sources
PubMed1996

Evidence for fluid volume depletion in hyponatraemic patients with bacterial meningitis.

Since the mechanisms underlying hyponatraemia in meningitis are poorly understood, we retrospectively reviewed the records of 187 paediatric patients with bacterial meningitis treated at the Department of Pediatrics, University of Bern, Switzerland, between 1982 and 1994. The degree of dehydration calculated from naked weight on admission and at 5 days was consistently (by 2.8 x 10(-2) and significantly more pronounced in 30 hyponatraemic (plasma sodium 130 mmol l-1 or less) than in 157 normonatraemic patients (plasma sodium 131 mmol l-1 or more). Furthermore, a tendency towards reduced sodium excretion was noted in hyponatraemic patients. The results suggest that in bacterial meningitis hyponatraemia is mostly induced by clinically latent fluid volume depletion.

Adolescent↗
PubMed1996

[Precision of glomerular filtration estimation by height/creatinine ratio in the child].

Formulae for estimating glomerular filtration rate with the use of body size, circulating creatinine, and an empirically derived constant are widely used. The aim of the present study was to determine whether these formulae enable accurate prediction of glomerular filtration measured from the labeled ethylenediaminetetraacetic acid in 843 pediatric patients. Bland-Altman analysis was performed on the measured glomerular filtration rate and that estimated using the constant developed in our laboratory. Age and sex of the 843 patients failed to consistently influence the empirically derived constant. Measured and estimated glomerular filtration rate were on the average identical. However, the 95% limits of agreement of the measured glomerular filtration rate with that estimated were wide (measured over estimated glomerular filtration from 0.53 to 2.04). Use of height to creatinine formulae to estimate glomerular filtration is therefore frequently insufficiently accurate.

Adolescent↗
PubMed1995

[Demonstration of mesangial IgA deposits in kidney biopsies of pediatric patients: comparison with the clinical picture].

Clinical and morphological findings were evaluated in 25 children with mesangial IgA deposits. 19 patients had recurrent macroscopic hematuria (n = 10), chronic proteinuria > 40 mg/(m2.h) (n = 5), recurrent hematuria with chronic proteinuria (n = 3), or chronic nephrotic syndrome (n = 1). The glomerular involvement was similar in six patients with history of Schönlein-Henoch purpura and in 13 patients without such history: normal or nearly normal glomeruli (n = 3), focal and segmental glomerulonephritis (n = 11) and diffuse proliferative glomerulonephritis (n = 5). End-stage renal disease developed in two patients with proteinuria > 40 mg/(m2.h) and more than 50% of their glomeruli are affected by crescents. The common histopathological features in patients with and without history of Schönlein-Henoch purpura suggest a common pathogenesis. The risk of poor outcome appears, related to the severity of proteinuria and to the presence of crescents, in more than 50% of glomeruli. Mesangial IgA deposits were also demonstrated in six children with steroid-responsive idiopathic nephrotic syndrome: light microscopic studies revealed normal or nearly normal glomeruli in five and focal segmental glomerular sclerosis in one patient. The microscopic findings were clearly different in the six patients with idiopathic nephrotic syndrome as compared with the patient with chronic nephrotic syndrome, who presented with severe glomerular lesions and extensive crescent formation. The results indicate that the presence of mesangial IgA deposits in the clinical setting of idiopathic childhood nephrotic syndrome is incidental and that such patients should still be considered as having idiopathic nephrotic syndrome in spite of their immunopathological features.

Adolescent↗
PubMed1995

[Antibiotic treatment of urinary tract infections in hospitalized children].

From 1980 to 1991 237 patients (aged 1 week to 15 years) with moderate to severe urinary tract infection had been treated at the Department of Pediatrics University of Berne, Switzerland. Bacterial etiology, antimicrobial in vitro susceptibility tests, and drug management were retrospectively analyzed. 266 bacterial pathogens were isolated from these patients. Escherichia coli was the most frequent etiologic agent (203), followed by Enterococcus (21), Klebsiella (20), Proteus (12), Pseudomonas (6), Enterobacter (2) and Serratia (2). The overall in vitro susceptibility of these isolates was 61% for aminopenicillins, 80% for co-amoxiclav, 83% for co-trimoxazole and 92% for aminoglycosides. Aminoglycosides were ineffective in vitro only against enterococci. However, since all enterococcal strains were always sensitive to aminopenicillins, none of the pathogens was concomitantly resistant to both aminoglycosides and aminopenicillins. Parenteral therapy had been given initially in 141 patients (59%); aminopenicillin and aminoglycoside in 105, and aminopenicillin alone in 36 cases (cefuroxime instead of aminopenicillin in some patients with suspected allergy to penicillin). 96 patients (41%) were initially treated with oral antibiotics (cotrimoxazole, aminopenicillin or co-amoxiclav). The initial antimicrobial regimen had to be modified in 31 cases (13%). In children with moderate to severe urinary tract infection prompt sterilization of urine and kidneys will prevent or suppress renal tissue lesions. The in vitro susceptibility results observed in the pathogens isolated in the patients prompt us to suggest that the above mentioned goal can only be achieved by an initial regimen consisting of an aminopenicillin and an aminoglycoside compound administered parenterally.

Adolescent↗
PubMed1995

Concealed administration of frusemide simulating Bartter syndrome in a 4.5-year-old boy.

A 4.5-year-old boy was admitted to three different hospitals because of a tendency towards dehydration and polyuria, along with normal blood pressure, hypochloraemia, hypokalaemia, metabolic alkalosis and an impaired urinary concentrating ability. A renal biopsy failed to reveal juxtaglomerular hyperplasia. The clinical and laboratory findings failed to improve despite supplementation with potassium chloride and treatment with indomethacin. The urine was found to contain frusemide. The parents denied any drug administration to the boy. The child is now doing well more than 1 year after separation from his mother. Since ingestion of diuretic cannot be differentiated from true Bartter syndrome by blood and urinary electrolyte measurements alone, a diuretic screen is warranted in children with findings consistent with Bartter syndrome.

Bartter Syndrome↗
PubMed1995

Urinary chloride excretion distinguishes between renal and extrarenal metabolic alkalosis.

UNLABELLED: The aetiology of normotensive hypokalaemic metabolic alkalosis is sometimes not obtainable from the history. Observations in adults indicate that the urinary chloride excretion is low in metabolic alkalosis of extrarenal origin. The chloride/creatinine ratio in random urines was therefore compared in 283 healthy children and in eight paediatric patients with metabolic alkalosis. The urinary chloride/creatinine ratio was reduced in four patients with metabolic alkalosis of extrarenal origin and within reference values or above in four patients with metabolic alkalosis of renal origin. CONCLUSION: The study confirms that urinary chloride/creatinine ratio discriminates between extrarenal and renal forms of metabolic alkalosis.

Adolescent↗
PubMed1995

Histological features of glomerular immaturity in infants and small children with normal or altered tubular function.

In children with renal tubular disorders the existence of retarded histological features of glomerular maturation has been suggested by our group. However, no valuable information is available on the frequency of histopathologically immature glomeruli in the normal kidney. For this reason we established a simple, semiquantitative definition of postnatal glomerular development: immature glomeruli (with at least half of the circumference of capillary loops densely lined with cuboidal epithelial cells), intermediate glomeruli (circumference of capillary loops lined with at least five adjoining cuboidal cells), and mature glomeruli. This definition was applied in a set of 71 normal kidneys from ages birth to 5 years. The relative frequency of the mentioned stages of glomerular maturation was strongly age dependent. In comparing the patients data with the normal findings it was possible to separate patients with the finding of disproportionately high fractions of immature glomeruli, provided the right age at biopsy is chosen. It is therefore concluded that the previous suspicion of late glomerular maturation may be validated in at least in some bioptic specimens.

Biopsy↗
PubMed1995

Normal prostaglandinuria E2 in Gitelman's syndrome, the hypocalciuric variant of Bartter's syndrome.

In familial Bartter's syndrome, hyperprostaglandinuria is considered a constant feature and prostanoid synthetase inhibition often positively influences the disease course. The urinary calcium excretion distinguishes two clinically and biochemically different variants, namely, classic Bartter's syndrome (normocalciuric or hypercalciuric variant; urinary calcium to creatinine > or = 35.3 mg/mg 10(-3)) and Gitelman's syndrome (hypocalciuric variant; urinary calcium to creatinine < 35.3 mg/mg 10(-3)). In the hypocalciuric variant of Bartter's syndrome prostanoid synthetase inhibition is of little benefit. Since the production of prostanoids has not been extensively studied in Gitelman's syndrome, the urinary excretion of prostaglandin E2 was assessed by radioimmunoassay in 11 untreated patients with Gitelman's syndrome (aged 10 to 21 years; five females and six males) and in 11 healthy controls (aged 11 to 20 years; five females and six males). The urinary excretion of prostaglandin E2 was similar in both study groups. The study provides the rationale for the poor effect of prostanoid synthetase inhibition in the hypocalciuric variant of Bartter's syndrome. The assessment of urinary excretion of prostaglandin E2 does not represent a diagnostic sine qua non in the context of familial Bartter's syndrome.

Adolescent↗
PubMed1995

Genetic heterogeneity in tubular hypomagnesemia-hypokalemia with hypocalcuria (Gitelman's syndrome).

To better clarify the genetic inheritance of primary tubular hypomagnesemia-hypokalemia with hypocalciuria, or Gitelman's syndrome (GS), we studied eight families (10 patients aged 11 to 22 years; 16 parents; 9 siblings) in which at least one offspring had GS (plasma magnesium < 0.65 mmol/liter; plasma potassium < 3.6 mmol/liter; high magnesium and potassium fractional excretions; molar urinary calcium/creatinine < 0.10). Two families each had two offspring of different sex with GS, who all had tetanic episodes and/or marked weakness during childhood or adolescence, whereas in three other families two mothers and three offspring presented GS and one father and two other offspring had hypomagnesemia and hypocalciuria but normal plasma potassium. The mean plasma magnesium and potassium levels of the patients of the first two families were significantly lower (P < 0.05) than those of the other three families. Intralymphocytic but not intraerythrocytic magnesium and potassium were significantly lower (P < 0.05) in patients compared to controls. We hypothesize that there are two different types of genetic transmission of GS, one autosomal recessive and one autosomal dominant with high phenotype variability. It seems that this genetic heterogeneity is associated with a different clinical expression with frequent tetanic episodes and lower plasma potassium and magnesium levels in the autosomal recessive form.

Adolescent↗
PubMed1995

Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis.

The acid-base balance of 199 patients with cystic fibrosis, seen from 1987 through 1992 at the Bern Outpatient Clinic, were evaluated. Simple metabolic alkalosis was demonstrated in 16 and mixed metabolic alkalosis and respiratory acidosis in 9 patients. When compared with 10 patients with simple respiratory acidosis and 16 with normal hydrogen ion balance, those with simple metabolic alkalosis were significantly younger. The need for pancreatic enzymes was significantly higher and the relative underweight significantly more severe in patients with either simple or mixed metabolic alkalosis and respiratory acidosis. The results indicate the rather common occurrence of chronic metabolic alkalosis in cystic fibrosis. It is observed in young patients, in patients who need high doses of pancreatic enzymes and in the those with poor nutritional status.

Acidosis, Respiratory↗
PubMed1995

Evidence for disturbed regulation of calciotropic hormone metabolism in gitelman syndrome.

Little attention has been paid to interactions between circulating levels of calcium, PTH, and 1,25-dihydroxycholecalciferol [1,25(OH)2D] and bone mineral density in primary renal magnesium deficiency. Plasma and urinary electrolytes, and circulating levels of calciotropic hormones were studied in 13 untreated patients with primary renal tubular hypokalemic alkalosis with hypocalciuria and magnesium deficiency. The blood ionized calcium concentration was significantly lower in patients than in controls. Despite this fact, PTH and 1,25-(OH)2D levels were similar in both groups of subjects. The negative linear relationships between PTH and ionized calcium, which significantly differed between Gitelman patients and healthy subjects in terms of intercept; the negative relationship between ionized calcium and 1,25-(OH)2D, which was comparable in both groups; and the positive relationship between 1,25-(OH)2D and PTH, which was identical in both groups, point both to a blunted secretion of PTH induced by magnesium depletion and to the lack of interference of the latter with the activation of 1 alpha-hydroxylase by PTH. The similar bone mineral density at the lumbar spine by dual energy x-ray absorptiometry in 11 patients and 11 healthy subjects argues against chronically sustained negative calcium balance.

Adolescent↗
PubMed1995

Outcome of idiopathic childhood nephrotic syndrome. A 20 year experience.

112 patients with idiopathic childhood nephrotic syndrome have been referred from 1970 through 1989 at the Department of Pediatrics, University of Berne. One patient remitted spontaneously without medication. Ninety-eight patients responded to prednisone: 15 had a single bout of nephrosis, 47 developed a tendency towards relapses and 36 steroid dependence. In 28 patients with tendency towards relapses cure took place on either prednisone alone or prednisone plus cyclophosphamide. In 18 patients with steroid dependency cure took place on prednisone alone or prednisone plus cyclophosphamide. Thirteen patients failed to respond to steroids. The course of the disease was more benign in 68 patients with minimal change disease as compared with 14 patients with focal and segmental glomerular sclerosis. Immunofluorescence studies demonstrated mesangial IgM deposits in 14 out of 54 patients, but this finding was not a marker for poor steroid response or progression to renal failure. The course of the disease was especially unfavourable in patients with persisting nephrosis on completion of the initial course of steroid therapy. In conclusion it appears appropriate to define the disease in terms of steroid responsiveness as steroid resistant patients sometimes show normal glomeruli, steroid responsive sometimes have focal and segmental glomerular sclerosis or mesangial IgM deposits, and decisions depend more on the steroid responsiveness than on the histological features.

Adolescent↗