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Biomedical subjects

F Sereni

Publications and source records attributed to F Sereni.

At least 19 recordsLinked to original sources
PubMed1998

Metabolic factors in the renal response to amino acid infusion.

In order to investigate the renal effects of amino acids (AA) with different metabolic fate, we compared the changes in glomerular and tubular function, nitrogen metabolism and glucoregulatory hormones in 7 volunteers during two infusions, one of a complete solution of amino acids (MIX-AA), which included five AA electively metabolized at the splanchnic level, and the other of a solution containing only essential AA (EAA), which escape splanchnic metabolism. MIX-AA increased GFR and RPF (from 104 +/- 6 to 122 +/- 13 and from 488 +/- 46 to 572 +/- 34 ml/min/1.73 m2), stimulated splanchnic metabolism as demonstrated by rises in urinary urea excretion (from 20.7 +/- 2 to 30.6 +/- 7.5 mg/min/1.73 m2) and the plasma glucagon/insulin ratio (from 21.4 +/- 13 to 26.7 +/- 15), and caused increases in fractional excretion of AA, FeNa and free-water clearance. During MIX-AA infusion significant correlations were observed between the individual values of GFR and the urea excretion rate (r = 0.66), and between GFR modifications (DeltaGFR) and the plasma glucagon/plasma insulin ratio (r = 0.40). No change in renal function, urea excretion and the glucagon/insulin ratio was observed with EAA. An intermediate splanchnic step (increased plasma glucagon/insulin ratio and ureagenesis) seems necessary in the pathway leading to the nonessential AA-induced rise in GFR; this might stimulate an ultimate intrarenal pathway (possibly involving the diluting segment) via a still undefined mechanism.

Adult↗
PubMed1996

The captopril test in children with renovascular and renal hypertension.

We used the captopril test (CT) in 32 children, 8 with renovascular hypertension (RVH), 17 with renal hypertension (RH) and 7 with normal blood pressure, in order to study the renin-angiotensin system activation (RASA). All children affected by RVH presented a positive CT: a post-captopril plasma renin activity (PRA) of 12 ng ml-1 h-1 or more, an absolute PRA increase of 10 ng ml-1 h-1 or more and a 150% increase or more, or 400% or more if the baseline PRA was less than 3 ng ml-1 h-1. The CT may be useful for demonstrating the RASA in RVH.

Adolescent↗
PubMed1996

Novel molecular variants of the Na-Cl cotransporter gene are responsible for Gitelman syndrome.

A hereditary defect of the distal tubule accounts for the clinical features of Gitelman syndrome (GS), an autosomal recessive disease characterized by hypokalemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria. Recently, we cloned the cDNA coding for the human Na-Cl thiazide-sensitive cotransporter (TSC; also known as ¿NCCT¿ or ¿SLC12A3¿) as a possible candidate for GS, and Simon et al., independently, described mutations in patients with GS. Now, we show 12 additional mutations consistent with a loss of function of the Na-Cl cotransporter in GS. Two missense replacements, R209W and P349L, are common to both studies and could represent ancient mutations. The other mutations include three deletions, two insertions, and six missense mutations. When all mutations from both studies are considered, missense mutations seem to be more frequently localized within the intracellular domains of the molecule, rather than in transmembrane or extracellular domains. One family, previously reported as a GS form with dominant inheritance, has proved to be recessive, with the affected child being a compound heterozygote. A highly informative intragenic tetranucleotide marker, useful for molecular diagnostic studies, has been identified at the acceptor splice site of exon 9.

Adult↗
PubMed1995

Percutaneous transluminal renal angioplasty in neurofibromatosis.

A 9-year-old boy with hypertension was found to have neurofibromatosis associated with stenosis of the right renal artery. Percutaneous transluminal angioplasty (PTA) was performed. Immediately post angioplasty angiography showed that the stenosis persisted, but over the next few days his blood pressure rapidly decreased and remained well controlled even when treatment was discontinued. The captopril stimulation test, performed after PTA, confirmed the return of plasma renin activity to normal values. A digital subtraction aortogram, performed 2.5 years after PTA, was unchanged. His blood pressure remained persistently normal, without anti-hypertensive agents. Based on these results, PTA is suggested as the first step in correcting renal artery stenosis due to neurofibromatosis. A complete anatomical resolution of the stenosis is probably not required since slight improvements in the renal artery lumen may be accompanied by important functional improvement.

Angioplasty, Balloon↗
PubMed1995

Macromolecular IgA and abnormal IgA reactivity in sera from children with IgA nephropathy. Italian Collaborative Paediatric IgA Nephropathy Study.

This multicenter study investigated the characteristics of circulating IgA molecules in 77 children: 42 had primary IgA nephropathy (IgAN), 20 were non-IgA glomerulonephritides (CGN) and 15 had urological problems (U). Fifteen assays were employed including the detection of macromolecular IgA [IgA immune complexes (IgAIC) by the conglutinin (K) assay, heavy molecular weight IgA in 2.5% polyethylene glycol (PEG), mixed IgA/IgGIC (Jacalin assay), IgA-Fibronectin (IgA-F) aggregates]IgA antibodies to alimentary antigens (gliadin, glycgli, glutein, ovalbumin, bovine serum albumin) and IgA binding to mesangial antigens (fibronectin, laminin, type IV collagen) or polycations (poly-L-lysine). Total IgA and IgA reacting with jacalin, supposed to bear an altered galactosylation, were measured as well. Mean levels of each kind of macromolecular IgA were significantly increased in children with IgAN in comparison to U disease (K-IgAIC p < 0.05, PEG-IgAIC p < 0.01, IgA/IgGIC p < 0.004, IgA-F aggregates p < 0.0003). However, IgA-F were the only macromolecular IgA significantly higher in IgAN than in CGN (p < 0.0005). IgA-F aggregates did not correlate with any urinary sign of activity, while K-IgAIC data were significantly related with microscopic hematuria (p < 0.05) and past history of gross hematuria (p < 0.02). Children with IgAN had mean levels of IgA reacting with the lectinic fractions of gliadin significantly higher than CGN (p < 0.01) and U groups (p < 0.003). IgAN displayed an enhanced production of IgA reacting with mesangial matrix components vs CGN (p < 0.03) and U (p < 0.0003) groups and showed altered interactions with positively charged molecules (poly-L-Lysine, p < 0.01) and carbohydrate residues (jacalin p < 0.05). In IgAN there is an increased circulation of altered IgA favouring the formation of macromolecular IgA, including true IgAIC or IgA aggregated by carbohydrate interactions. The affinity for the mesangial matrix glycoproteins and for the mesangial area electrical charge might further enhance the trapping and deposition of the immune material containing IgA. IgA-F aggregates seem to be a marker of this event, while complement binding molecules in IgAIC correspond to the hematuric manifestation of the nephritogenic process.

Adolescent↗
PubMed1994

[IgA serology in idiopathic IgA deposit nephropathy in children].

It is generally thought that in primary IgA nephropathy (IgAN) an altered immune response favours high levels of serum IgA directed against environmental or mesangial antigens (Ag) leading to circulating IgA containing immune complexes (IgAIC). The aim of this multicenter collaborative study was to evaluate some of the IgA immunologic abnormalities in children with IgAN. We investigated 42 children with biopsy-proved IgAN, 21 children with non-IgA glomerulonephritides (CD) and 15 with previous urologic disorders without any evidence of immunologic disease (U). The following methods were used: detection of macromolecular IgA (IgAIC by the conglutinin solid-phase assay, heavy MW IgA measured in 2.5% polyethylene glycol precipitate, IgA-fibronectin aggregates, mixed IgA-IgGIC); serum levels of IgA to alimentary Ags (gliadin, glyc-gli, ovalbumin, bovine serum albumin) and mesangial Ags (fibronectin, laminin, type IV collagen) and reactivity of IgA with the lectin jacalin. In children affected with IgAN serum levels of macromolecular IgA were significantly higher in comparison to U group (p < 0.05-p < 0.0005). IgA-fibronectin aggregates only were significantly higher also than CD group (p < 0.0005). Mean levels of antigliadin IgA were significantly higher in IgAN than in controls (CD p < 0.01 and U p < 0.03) and similar data were found for IgA to mesangial matrix (laminin and fibronectin), which were significantly greater in IgAN than in CD and U (p < 0.01-p < 0.0002). Serum IgA in children with IgAN showed a greater affinity for both polycations and glycosylated molecules. Children affected by IgAN present abnormalities in serum IgA similar to those observed in adults with the same disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Genetic models of arterial hypertension--role of tubular ion transport.

The description of pathogenetic mechanisms underlying different genetic models of essential hypertension is a useful way of illustrating the logical sequence needed to dissect a complex phenotypic condition such as hypertension. The abnormalities in renal function observed in spontaneously hypertensive rats of the Okamoto strain and Milan strain will be emphasized. The description may proceed "downward" from alterations that affect the whole body function to cellular and subcellular levels. However, the identification in the Milan strain rats of a point mutation in the gene coding for adducin, a skeletal protein able to modulate transepithelial sodium transport, provides the opportunity to reconstruct, in an "upward" direction, the sequence of events leading from the single point mutation to the final complex phenotype of essential hypertension.

Animals↗
PubMed1993

Renal effects of cyclosporin A in children treated for idiopathic nephrotic syndrome.

Little data have been published on tubular renal function during cyclosporin A treatment in children without transplants. We studied 12 young subjects (mean age 10 years) with steroid-responsive idiopathic nephrotic syndrome and with signs of steroid toxicity. After achieving remission with prednisone 60 mg/m2, 8 children started cyclosporin A therapy (6 mg/kg/day) (group A) and 4 children were given cyclophosphamide 2.5 mg/kg/day (group B). The latter were considered as controls together with 10 other children with idiopathic nephrotic syndrome in complete remission and off therapy (group C). We monitored creatinine clearance and tubular handling of beta 2-microglobulin, sodium, phosphorus and uric acid for one year. Cyclosporin A induced a decrease in creatinine clearance with a decrease in fractional excretion of beta 2-microglobulin; sodium excretion was similar in the two treated groups and a transient decrease in fractional excretion of uric acid was seen only in patients receiving cyclosporin A. Both groups showed an increased renal threshold phosphate concentration. Our results suggest that in children, cyclosporin A therapy induces a decrease in glomerular filtration rate associated with increased reabsorption activity of proximal tubular cells.

Adolescent↗
PubMed1991

Increased renal tubular Na-K-ATPase activity in Milan hypertensive rats in the prehypertensive period.

Milan hypertensive (MSH) rats develop hypertension around the 3rd-4th week of life and exhibit increased Na-pump activity in adulthood. The present study was performed to evaluate whether or not hypertension is preceded by an increase in Na-K-ATPase activity. Total and ouabain-sensitive ATPase activities were studied in single microdissected medullary thick ascending limb of Henle (mTAL) tubules from MHS, Milan normotensive (MNS) and Sprague-Dawley (SD) rats at 22-24, 26-28 and 45-60 days of age. Data are given as mean +/- SEM. Total and Na-K-ATPase activity exhibited a developmental pattern in MHS, MNS and SD rats. At 22-24 days no difference was seen between MHS and MNS animals. At 26-28 days MHS had a higher total and Na-K-ATPase activity than MNS (3031 + 171 vs 2471 + 178 pmol phosphate/mm tubule per hour, P less than 0.05; 2289 + 205 vs 1653 + 151, n = 10, P less than 0.05). At this age there was still no difference in mean arterial blood pressure (88 + 4 vs 86 + 3 mm Hg, n = 15). Adult MHS rats had higher blood pressure (140 + 9 vs 112 + 8 mm Hg, P less than 0.001) and higher total (3544 + 136 vs 2718 + 215 pmol phosphate/mm tubule per hour, n = 10, P less than 0.01) and Na-K-ATPase activity (2670 + 99 vs 1942 + 217 pmol phosphate/mm tubule per hour, n = 10, P less than 0.05) than adult MNS rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Familial aggregation of blood pressure in a paediatric population.

Familial aggregation of blood pressure in childhood and the difference between males and females were studied in a random sample of a nursery and school-age population in Milan. Age, sex, height, weight, skinfold thicknesses and heart rate were obtained. Blood pressure was measured in accordance with the recommendations of the Task Force of Blood Pressure Control in Children. After adjusting for age, significant correlation coefficients were found between mother and son (r = 0.17 and r = 0.11), mother and daughter (r = 0.11 and r = 0.15), and father and son (r = 0.16 and r = 0.17) for systolic and diastolic pressure, respectively; the father-daughter correlations were not statistically different (r = 0.08 and r = 0.03). Multiple regression analysis underlined the difference between males and females; height was an important determinant in the males and body weight in the females. In conclusion, anthropometric measurements should be considered in evaluations of blood pressure status. Our results suggest important differences between males and females. The BP pattern of the parents also seems more important for sons, and there seems to be a lower correlation between fathers and daughters.

Adult↗
PubMed1989

Na,K-ATPase activity in renal tubule cells from Milan hypertensive rats.

Several abnormalities of cation transport have been described in the Milan hypertensive rats (MHS). In this study we examined Na,K-ATPase activity in proximal convoluted tubules (PCT) cells and medullary thick ascending limb of Henle cells (TAL) from MHS and from the Milan normotensive rats (MNS). Na,K-ATPase activity was determined as 32P-ATP hydrolysis in single tubule segments. Na,K-ATPase activity (pmol Pi/mm t/h) was significantly higher in MHS than MNS both in PCT (903 +/- 227 n = 8 v 506 +/- 285 n = 12) and TAL (4324 +/- 800 n = 5 v 3063 +/- 625 n = 5). Na,K-ATPase dependent respiration was determined in PCT cell from MNS and MHS. Under basal condition Na,K-ATPase dependent respiration (mumol O2/mg protein/h) was higher in MHS than in MNS (24.2 +/- 1.8 n = 5 v 16.1 +/- 0.4 n = 5). When the cells were Na loaded by amphotericin Na,K-ATPase dependent respiration increased significantly more in MHS than MNS (38.4 +/- 1.6 v 26.8 +/- 2.2 n = 4). Thus, Na,K-ATPase activity is higher in renal tubule cells both at normal intracellular Na and after the cells have been Na loaded. The results indicate that regulation of Na homeostasis in renal tubule cell is different in MHS and MNS.

Amphotericin B↗
PubMed1985

Correlation between fetal and maternal serum bile acid concentrations.

Serum concentrations of different bile acids (BA) were determined by radioimmunoassay in 56 human fetuses and mothers. Serum was obtained immediately after legal abortion, performed between the 14th and the 21st wk of gestation. Conjugated cholic (CCA) and chenodeoxycholic acid (CCDCA) concentrations were determined in 33 cases, conjugated lithocholic (CLCA) and deoxycholic acid (CDCA) in 20, and sulfolithocholyglycine (SLCG) in 15. In fetal blood, mean concentrations of CCA (0.80 +/- 0.40 mumol/liter), CCDCA (4.50 +/- 2.70 mumol/liter), and CLCA (1.70 +/- 1.04 mumol/liter) were significantly higher than those in the mother (CCA 0.34 +/- 0.17 mumol/liter; CCDCA 0.79 +/- 0.34 mumol/liter; CLCA: 0.70 +/- 0.30 mumol/liter; p less than 0.001); fetal serum levels of CDCA (0.46 +/- 0.32 mumol/liter) and SLCG (0.15 +/- 0.09 mumol/liter) were lower than in the mothers (CDCA 1.20 +/- 0.80 mumol/liter, p less than 0.001; SLCG 0.40 +/- 0.30 mumol/liter, p less than 0.01). There was no correlation between levels of BA and gestational age. Serum total protein and albumin concentrations were both reduced in 10 fetuses as compared with the mothers. These data support the concept of a state of physiologic cholestasis during development and suggest that placental transfer of primary BA occurs mostly in the fetal to maternal direction. This transfer could be facilitated by the reduced fetal plasma albumin concentration, since BA in free solution diffuse more easily through the placenta. There is evidence of lithocholic acid synthesis in the fetal liver, while deoxycholic acid appears to be mostly of maternal origin. Finally, sulfation of BA is poorly developed at this age of gestation.

Bile Acids and Salts↗
PubMed1983

Immune response to hepatitis B vaccine in staff and patients in renal dialysis units.

Anti-HBs response was detected in 96 per cent of staff members in three haemodialysis units after three 20 microgram doses of hepatitis B vaccine and in 82 per cent of adult patients treated with three 40 microgram doses. The percentage of responders and levels of antibody remained unchanged at 12 months from the beginning of the trial. Three out of six children injected with three 20 microgram doses in a paediatric haemodialysis unit remained free from markers of HBV infection and had high levels of anti-HBs after the second dose of vaccine. The other three children who developed serological markers of HBV infection seroconverted to anti-HBc within six months from the first dose and, in one of them, antigenaemia at three and four months was detected.

Adult↗