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Biomedical subjects

U Simeoni

Publications and source records attributed to U Simeoni.

At least 19 recordsLinked to original sources
PubMed1995

Auxiliary liver transplantation for fulminant and subfulminant hepatic failure.

We report the first series of 9 auxiliary liver transplantations performed as a bridge to recovery in 8 patients with fulminant and subfulminant hepatic failure. Hepatic failure was due to hepatitis A virus (n = 3), hepatitis B virus (n = 1), hepatotoxic drugs (n = 2), autoimmune disease (n = 1), or it was of unknown origin (n = 1). The donor liver was reduced to a left lobe (n = 2), a left liver (n = 4), or a right liver (n = 3), and was implanted in an orthotopic position beside the native liver after it was resected by a left or a right hepatectomy. Conventional immunosuppression was used to prevent rejection. Six patients regained normal consciousness within 2 weeks, without any sequelae. Two patients had persisting encephalopathy due to graft initial dysfunction, one of whom showed portal vein thrombosis, which was successfully cleared. The other one showed hepatic vein stenosis and was retransplanted at day 15. Five of eight patients had to be reoperated because of a surgical complication. Five patients showed rapid regeneration of their native liver, but one died at day 45 from severe herpes virus broncholitis. The auxiliary grafts were removed (n = 3) or left to atrophy by tapering immunosuppression (n = 1). One patient developed cirrhosis of the native liver and died of infectious complications at day 42. The native livers of the two remaining patients are still atrophic, one at 4 months and one at 1 month posttransplant. Finally, 6 of 8 patients are alive with a follow-up of 1 to 17 months. Four of them have permanently stopped their immunosuppressive therapy. Our experience demonstrates that auxiliary orthotopic liver transplantation (1) is feasible in children and adults, using either a left or a right liver graft, (2) is efficient in providing adequate liver function, and (3) gives a real chance to the native liver to regenerate, offering these patients a future free of immunosuppression.

Adolescent↗
PubMed1994

Involvement of nitric oxide in the vasodilatory response to parathyroid hormone-related peptide in the isolated rabbit kidney.

1. The present study was designed to explore the role of NO derived from L-arginine in the vasodilatory response to synthetic human parathyroid hormone-related peptide-(1-34) in the isolated rabbit kidney perfused in the presence of indomethacin (10 mumol/l) and preconstricted with noradrenaline (7.2 nmol/min). 2. Under control conditions, bolus administrations of acetylcholine (10 mumol/l), an NO-dependent renal vasodilator, verapamil (0.1 mmol/l), an NO-independent renal vasodilator, and parathyroid hormone-related peptide (87 nmol/l) decreased the preconstriction pressure, by 31%, 71% and 43%, respectively. 3. Bolus administration of 100 mumol/l NG-nitro-L-arginine-methyl ester caused a 20% increment in the perfusion pressure of the noradrenaline-preconstricted kidney. NG-nitro-L-arginine methyl ester inhibited the vasodilatory effect of acetylcholine and parathyroid hormone-related peptide, by 68% and 44%, respectively, but did not alter the verapamil-induced vasodilatation. 4. Unlike L-arginine, the bolus administration of 1 mumol/l of a mono-substituted L-arginine derivative, N-alpha-benzoyl-L-arginine ethyl ester, durable decreased the noradrenaline/NG-nitro-L-arginine methyl ester-induced preconstriction by 57%. 5. Both L-arginine and N-alpha-benzoyl-L-arginine ethyl ester effectively reversed the inhibition induced by NG-nitro-L-arginine methyl ester on the vasodilatation elicited by acetylcholine and parathyroid hormone-related peptide. 6. In conclusion, the formation of NO from L-arginine contributes a substantial part to the vasodilatory action of parathyroid hormone-related peptide. Therefore, parathyroid hormone-related peptide appears to have a place among the renal haemodynamically active substances, whose vasodilatory actions are tuned by NO.

Acetylcholine↗
PubMed1994

Specific developmental profiles of lysosomal and brush border enzymuria in the human.

Various enzymatic urinary activities have been proposed to assess renal proximal tubule damage in children, including neonates. Nevertheless comprehensive knowledge on the developmental aspects of physiological enzymuria is limited, particularly with regard to lysosomal and brush border enzymuria. Urinary activities of two lysosomal enzymes, N-acetyl-beta-D-glucosaminidase (NAG) and beta-galactosidase (GAL), and of two brush border enzymes, alanine aminopeptidase (AAG) and gamma-glutamyltransferase (GGT) were comparatively investigated in normal prematures (n = 28), term neonates (n = 52), infants aged less than 2 years (n = 19) and children (n = 33), and compared to urinary excretion of beta 2-microglobulin (B2M). Enzymatic activities were assayed using either spectrophotometrical (NAG, AAP, GGT) fluorimetrical (GAL) or radioimmunological (B2M) methods, and were related to urinary creatinine excretion. Developmental profiles of both the studied lysosomal enzymes and of B2M were similarly characterized with significantly decreasing values from prematures (NAG 9.29 +/- 1.44, GAL 2.26 +/- 0.26 IU/mmol creatinine, indicated as mean +/- SEM) to term neonates (6,94 +/- 0.58 and 1.76 +/- 0.15 IU/mmol creatinine, respectively) and older infants and children. Lysosomal enzymatic urinary activities correlated linearly with a coefficient of r = 0.75, (p < 0.05), while correlations between each lysosomal enzymatic activity and B2M urinary excretion were weaker.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1994

[Gitelman syndrome in children: true hypokalemia but false Bartter syndrome].

BACKGROUND: Gitelman's syndrome or familial hypokalemia-hypomagnesemia and Bartter syndrome share some common features but their prognosis is quite different. CASE REPORT: Four unrelated children, aged 5 to 12 years, were studied because they suffered from muscle cramps and/or abdominal pain. Supportive findings included: hypokalemia (2.1 to 2.9 mmol/l), metabolic alkalosis (31 to 34 mmol/l), hyperkaliuresis (5.8 to 7.1 mmol/kg/day), hypomagnesemia (0.58 to 0.64 mmol/l), hypermagnesuria (0.19 to 0.23 mmol/kg/day), hypocalciuria (0.012 to 0.021 mmol/kg/day). Blood pressure contrasting with high renin activity (19.04 to 20.03 ng/ml/hr) was normal. Chloride fractional excretion after oral water supplementation was only slighty decreased and hypercalciuric response to furosemide administration was not observed. Supplementation with magnesium chloride failed to correct hypomagnesemia while potassium chloride improved hypokalemia. CONCLUSIONS: Age of onset, tetany manifestations, absence of growth retardation, hypermagnesuria despite, hypomagnesemia, hypocalciuria not improved by furosemide favor the diagnosis of Gitelman's syndrome rather than that of Bartter syndrome initially considered.

Bartter Syndrome↗
PubMed1993

Evidence for adenylyl cyclase-dependent receptors for parathyroid hormone (PTH)-related protein in rabbit kidney glomeruli.

Studies were conducted to test whether parathyroid hormone-related protein (PTHrP) is able to stimulate adenylate cyclase activity in isolated rabbit glomeruli. Maximal stimulations were reached at 10(-7) M of human PTHrP-(1-34) or rat PTH-(1-34) and showed a 3-3.3 fold increase over basal activity. The potency (EC50) values were close to 10(-9) M. The guanyl nucleotide GTP, at 10(-5) M, potentiated the effect of PTH and PTHrP but reduced their potency. The combined effect of maximal concentrations of PTHrP and PTH was not additive, and the PTH antagonist [Nle8.18, Tyr34]-bPTH-(3-34)amide inhibited both PTHrP- and PTH-stimulated adenylate cyclase activities. These findings suggest that PTHrP could affect glomerular function through changes in glomerular cAMP content by interaction with PTH receptors.

Adenylyl Cyclases↗
PubMed1993

Renin stimulating properties of parathyroid hormone-related peptide in the isolated perfused rat kidney.

Previous studies showed that PTHrP exhibits renal vasodilating, arteriolar cAMP stimulating and receptor binding properties. The present experiments were designed to study whether PTHrP may influence renin secretion. Rat kidneys were isolated and single-pass perfused at constant flow and stabilized pressure. Exposures to PTHrP or PTH stimulated a dose-dependent renin release reaching similar Vmax. The affinity (0.1 nM) and threshold concentration (0.01 nM) for PTHrP were about 10 times lower than for PTH. Compared to 10 microM isoproterenol, the maximum renin responses to PTHrP were similar but of shorter duration. The PTHrP dose-response curve was not affected by 10 microM indomethacin. Administered simultaneously, PTHrP and PTH displayed no additive effects. PTHrP-induced renin release as well as the role of extracellular calcium were further studied in nonfiltering kidneys, which were perfused at a constant flow and stable pressure in a closed circuit. Basal renin release was inversely related with perfusate calcium and was depressed by the calcium ionophore BAY-K8644. PTHrP (100 nM) induced a 1.6-fold increase of basal renin release in normocalcic perfusate. Removing calcium abolished renin responses. PTHrP reversed the inhibiting effects of hypercalcic media or BAY-K8644 on basal renin release. The results support calcium-mediated renin stimulating properties for PTHrP, via PTH receptors, independently from baroreceptors, macula densa and prostaglandins.

Animals↗
PubMed1993

Stimulatory action of parathyroid hormone on renin secretion in vitro: a study using isolated rat kidney, isolated rabbit glomeruli and superfused dispersed rat juxtaglomerular cells.

1. We have previously reported that pharmacological concentrations (125nmol/l) of parathyroid hormone may stimulate renin release in the stable recirculating and non-filtering isolated rat kidney. 2. In the present study we have attempted to extend these initial observations by examining the concentration-related response of renin release to parathyroid hormone, using the same model of isolated kidney, and determining whether the effect of parathyroid hormone on renin release can be demonstrated by more direct approaches. Thus, the effects of parathyroid hormone on renin secretion were investigated in two other renal preparations: isolated rabbit glomeruli and isolated rat juxtaglomerular cells. 3. In the isolated kidney, rat parathyroid hormone significantly stimulated renin accumulation in the perfusate in a concentration-related manner with a threshold of 1 nmol/l. 4. In both glomeruli and juxtaglomerular cells bovine [Nle8,18,Tyr34]parathyroid hormone-(1-34)amide effectively and repeatedly stimulated renin release. These results imply that there is a direct stimulatory effect of parathyroid hormone on renin release. 5. We also examined the effect of [Nle8,18,Tyr34]parathyroid hormone-(1-34)amide during extracellular calcium buffering in the glomeruli. [Nle8,18,Tyr34]parathyroid hormone-(1-34)amide was uneffective in calcium-free medium. Increasing the extracellular ionized calcium concentration to 2.5 mmol/l increased the extent of stimulation in accordance with the reported ability of parathyroid hormone to block calcium channels and relax vascular smooth muscle cells. 6. These results provide further support for the role of parathyroid hormone as a direct mediator of renin secretion; moreover, the renin-stimulating action of parathyroid hormone may be mediated through the inhibition of calcium influx.

Animals↗
PubMed1992

Phosphate dialytic removal: enhancement of phosphate cellular clearance by biofiltration (with acetate-free buffer dialysate).

Phosphate dialytic removal (PDR) depends in part on the type (acetate or bicarbonate) and the concentration of the buffer dialysate. Plasma phosphate reduction or PDR during a dialysis treatment is the algebraic sum, of phosphate cellular flux (removal or captation) and of phosphate tissular precipitation. High bicarbonate levels induce an intracellular shift of phosphate, thus not available for dialytic removal. On the contrary, acidosis prevents P shifting into the intracellular space, thus more P is available for dialytic removal. In order to evaluate cellular phosphate sequestration (CPS) we tested PDR in a crossover study. Three children were dialyzed (18 sessions) successively using either biofiltration with free buffer dialysate and a constant bicarbonate fluid infusion rate (BF) or using sequential biofiltration (SBF) with an initial controlled acidosis period realized by bicarbonate reinjection fluid rate modelling. PDR was higher in SBF (32 +/- 4 mmol/session) than in BF (24 +/- 6 mmol/session). SBF seemed to be efficient against CPS; it clearly demonstrates that bicarbonate modelling is a promising dialytic approach to enhance PDR. The real clinical relevance of these biological results needs clinical long-term evaluation.

Adolescent↗
PubMed1992

[Acute kidney failure and nutrition].

Acute renal failure (ARF) is characterized by a persistently high mortality rate, mainly in prerenal, postaggressive forms. Nutritional perturbations are related to the metabolic response to stress, ie mainly an elevation of the basal caloric expenditure and a marked proteic hypercatabolism, and to specific consequences of the loss of renal function. Identification of characteristic metabolic patterns and of their mediators, leading to a nutritional support adjusted to the elevated demand rather than to the impairment of renal excretion faculties, may improve the prognosis. Benefits of such a nutritional support may be restricted to hypercatabolic forms of ARF in the intensive care unit, provided extrarenal failures are reversible.

Acute Kidney Injury↗
PubMed1991

Solute equilibration curves, crossing time for urea and glucose during peritoneal dialysis: a function of age in children.

Glucose is absorbed from the dialysate more rapidly in younger than in older children on CAPD leading to a relatively early loss of ultrafiltration during dwell time. In order to assess peritoneal permeability and in term to prescribe optimal management of CAPD, we tested peritoneal equilibration curves (EC) for urea and glucose, especially the crossing time point of these two ECs. Baseline values were obtained from 8 patients divided in two groups by age at start of CAPD: group I (N = 4) mean age 1 year 6 months, mean body weight 8.25 +/- 3.17 kg, group II (N = 4) mean age 12 years 6 months, mean body weight 33.5 +/- 1.5 kg. The crossing time point is earlier in group I (49 +/- 14 min) than in group II (101 +/- 20 min) (p less than 0.001). Followup of each patient, during a mean time of 20 months in group I and 23 months in group II, establishes that the curves crossing time point for each patient remains stable.

Age Factors↗
PubMed1991

[Double profile dialysis: ultrafiltration and sodium variable description and clinical validation in the child].

Despite significant technical improvements (bicarbonate dialysate, volumetric ultrafiltration control) high intradialytic ultrafiltration is troublesome in children, specially in the proportion of patients presenting a normal or low blood pressure even with overweight. We used, in this group of children (overhydratated without vascular repercution) a modelling of both sodium and ultrafiltration during dialysis, in order to achieve dry body weight without increasing session time despite hypotension risks. The usefulness and practicability of sodium and ultrafiltration modelling together during dialysis in children is analysed in a short time study (for plasma volume changes calculation) and in a long term follow up study over a year (for clinical tolerance). Today, we reserve this form of dialysis only for a single session needed by overhydratation (more than 5% of dry body weight) in order to achieve dry body weight maintaining dialysis session time constant without increasing side effects (hypotension).

Blood↗
PubMed1991

[En bloc transplantation of liver, stomach, pancreas and small intestine in an infant. Apropos of a case].

The now common practice of joint kidney and pancreas or heart or lung transplantation is being completed by other combinations. This is shown by our case of en bloc liver-pancreas-stomach-duodenum-small bowel transplantation in an 18-month-old infant with small bowen atresia complicated by biliary cirrhosis secondary to total parenteral feeding, after the failure of an intraperitoneal visceral transplant at 1 year of age. The graft was taken from an 8-year-old donor and was not pretreated. Being made of the whole intraperitoneal visceral mass, it had to be adapted to the recipient's size by ex vivo exeresis of the right liver, of the spleen, of the terminal ileon and of the colon. Following intraperitoneal visceral exenteration in the recipient, the graft was inserted in an orthoptic position with a digestive reconstruction by esogastric anastomosis and terminal ileostomy. Immunosuppression combined steroids, azathioprine, ciclosporine, and the biological and immunological follow-up regarded the hepatic and pancreatic functions. The intestinal graft was controlled by repeated biopsies through the stomy. Rectal biopsies and lymphocyte typing in the peripheral blood allowed watching for the occurrence of a possible graft-versus-host disease. The outcome was marked by the persistence of massive lymphorrhea during three months and severe central neurological disorders caused by the difficulties to adapt the level of ciclosporine. The hepatic and pancreatic functions became normal within a few days, and the intestinal function allowed progressively suppressing parenteral feeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗