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S Favaro

Publications and source records attributed to S Favaro.

At least 37 records · Page 2Linked to original sources
PubMed1995

Endothelium-derived vasoactive substances in Bartter's syndrome.

An imbalance between endothelium-derived vasoactive substances such as endothelin and endothelium-derived nitric oxide (NO) might be viewed as a possible determinant of vascular hyporeactivity. To check this possibility the authors evaluated the role of endothelin and NO in the reduced vascular reactivity of Bartter's syndrome. Plasma immunoreactive endothelin (22.07 +/- 7.06 vs 13.80 +/- 1.43 pmol/L, P < 0.011), urinary excretion of NO2- (0.28 +/- 0.10 vs 0.15 +/- 0.02, mumol/mumol of urinary creatinine, P < 0.01) and NO3- (0.17 +/- 0.07 vs 0.09 +/- 0.02 mumol/mumol of urinary creatinine, P < 0.011), and forearm resting blood flow (FRBF) (6.67 +/- 1.69 vs 4.30 +/- 0.38 mL/m'/100 mL, P < 0.005) were increased in patients with Bartter's syndrome in comparison with normal controls (C). No difference in postischemic maximal FBF was found (34.14 +/- 4.67 vs 31.35 +/- 2.86 mL/minute/100 mL), while patients showed a slower recovery after peak flow (PF) (77.57 +/- 61.35 vs 9.42 +/- 3.69 seconds, P < 0.013). Higher plasma endothelin supports the defect in vascular reactivity of Bartter's syndrome already shown for angiotensin II and norepinephrine and is in keeping with the altered intracellular calcium signaling previously demonstrated by the authors in this syndrome. The increased excretion of NO2- and NO3- in this syndrome, together with the higher FRBF and the slower recovery of the FBF and PF, argues in favor of an increased NO synthesis in Bartter's syndrome and of assigning it a role in the vascular hyporeactivity of Bartter's syndrome.

Adolescent↗
PubMed1994

Renal synthesis of prostaglandins and thromboxane has no causative role for protein-induced glomerular hyperfiltration in healthy humans.

The study was devised to establish the role of prostaglandin E2, prostaglandin1 alpha and thromboxane A2 in the genesis of glomerular hyperfiltration response to a meat meal in healthy humans. To this end, a group of 8 healthy women was studied 4 times: in the control state (study 1), after a meat meal (study 2), following a meat meal associated with intravenous aspirin (study 3) and finally after a meat meal associated with intravenous aspirin following 2-day pretreatment with oral aspirin (study 4). Urinary excretion of prostaglandins and thromboxane increased during the glomerular hyperfiltration response to a meat meal and was suppressed by aspirin administration which did not suppress the renal hemodynamic response to the meat meal. The data do not support a causal role for prostaglandins and thromboxane A2 in the hemodynamic response to acute protein loading.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Renal prostaglandins and thromboxane A2 lack a functional significance in the genesis of protein-induced glomerular hyperfiltration in human renal disease.

The study was devised to assess the effects of a protein load (2 g/kg BW) on urinary prostaglandin E2 (PGE2), 6-keto-PGF1 alpha and thromboxane A2 (TxA2) in patients with renal failure of glomerular origin. To this end, 8 women with a glomerular filtration rate of 55 +/- 12 ml/min x 1.73 m2 underwent the following studies: study 1: control; study 2: meat meal; study 3: meat meal+intravenous aspirin; study 4: pretreatment with oral aspirin for 2 days+protocol in study 3. Glomerular hyperfiltration was seen after the meat meal (study 2) and was not suppressed by aspirin (studies 3 and 4). Urinary PGE2, 6-keto-PGF1 alpha and TxA2 increased after the meat meal in study 2 and were suppressed by aspirin in studies 3 and 4. The ratio between vasodilative (PGE2 + 6-keto-PGF1 alpha) and vasoconstrictive (TxA2) autacoids increased during the meat meal (study 2) and was suppressed when aspirin was injected at the time of the oral protein load, thus, the effect of aspirin was much greater for PGE2 and PGF1 alpha than for TxA2. These data do not support that urinary prostaglandin and TxA2 have a direct role in renal hyperfiltration due to an acute protein load.

Adult↗
PubMed1987

Resting and stimulated cytosolic free calcium levels in neutrophils from patients with Bartter's syndrome.

Cytosolic free calcium concentrations ([Ca2+]i) were measured in resting and chemotactic peptide-activated neutrophils from eight patients with Bartter's syndrome and compared with levels determined in neutrophils isolated from healthy controls. [Ca2+]i was measured with the intracellular trappable fluorescent indicator Quin2. The synthetic tripeptide formylmethionyl-leucyl-phenylalanine (fMet-Leu-Phe) was used as a stimulant. No difference was found in resting [Ca2+]i between neutrophils from normal controls and those from patients with Bartter's syndrome. On the contrary increases in [Ca2+]i stimulated by fMet-Leu-Phe concentrations higher than 10(-8) mol/l were significantly less in neutrophils from patients with Bartter's syndrome. It is suggested that neutrophils from patients affected by Bartter's syndrome exhibit an intrinsic anomaly in the mechanism responsible for intracellular Ca2+ mobilization.

Adolescent↗
PubMed1986

Peripheral lymphocyte subsets in human chronic pyelonephritis.

Comparative study of peripheral blood lymphocyte surface markers in chronic pyelonephritis (CP) and chronic glomerulonephritis (GN) patients, and in normal controls showed no differences between controls and GN patients. In CP patients, a significant absolute increase in B cells, and an absolute decrease in T cells were observed as well as significantly lower and higher percentages of OKT4 and OKT8 cells, respectively, leading to a decrease in the OKT4/OKT8 ratio. Furthermore, the percentage of large granular cells was significantly higher in CP patients, while no differences in TIa cells emerged. The overall picture shown by the CP patients is compatible to a cell-mediated immune (CMI) response defect.

Adolescent↗
PubMed1984

[Role of Tamm-Horsfall mucoprotein in calcium oxalate lithogenesis].

Tamm-Horsfall (TH) mucoprotein has been suggested to play a lithogenetic role in calcium-oxalate nephrolithiasis. However it is still debated whether it promotes or inhibits crystal growth and aggregation. To make clear the role played by this mucoprotein, we have carried out the following experiments: 1) the urinary excretion of TH has been evaluated by radial immunodiffusion in 27 recurrent idiopathic CaOx stone formers and in 35 controls; 2) in a metastable solution of CaOx the effect of TH addition on crystal growth has been monitored; 3) in whole urine the effect of TH addition on crystal aggregation has been assayed by an aggregometer. Urinary excretion of TH is significantly lower in stone formers. TH does not seem to promote crystal growth, while it is effective on crystal aggregation. These data seem to suggest that the reduced excretion of TH in nephrolithiasis may be a lithogenic risk factor.

Calcium Oxalate↗
PubMed1983

Juvenile renal stone disease: a study of urinary promoting and inhibiting factors.

Urinary excretion of the most widely studied renal stone promoting (calcium, oxalate, uric acid and phosphate) and inhibiting (citrate, magnesium, pyrophosphate and glycosaminoglycans) factors, as well as the Tamm-Horsfall mucoprotein, was evaluated in 14 children with idiopathic calcium nephrolithiasis, 6 children with renal stone disease secondary to excretory malformations and 19 normal controls. No statistically significant differences in urinary excretion of promoting and inhibiting factors were found in children with idiopathic calcium nephrolithiasis but the relationship between promoting and inhibiting factors was changed as shown by an abnormal ratio of oxalate/citrate X glycosaminoglycans. This finding suggests that there is an imbalance between promoting and inhibiting factors in children with idiopathic calcium nephrolithiasis, and it is not detected by assay of each single substance.

Adolescent↗
PubMed1983

Increased urinary excretion of renal enzymes in idiopathic calcium oxalate nephrolithiasis.

Urinary excretion of gamma-glutamyl transpeptidase, angiotensin I converting enzyme, beta-galactosidase and N-acetyl-beta-glucosaminidase was evaluated in 30 patients with idiopathic calcium oxalate urolithiasis. Higher than normal values were observed and the excretory enzyme pattern suggested tubular damage in patients with stones. A parallel study in the rat showed that an oxalate surcharge can promote increased urinary excretion of these enzymes. It is known that urothelium injury may enhance crystal adhesion. If the damage is primary it may be viewed as a promoting factor. If it is secondary it may be considered a factor capable of increasing salt precipitation.

Acetylglucosaminidase↗
PubMed1983

Prevalence of hyperoxaluria in idiopathic calcium oxalate kidney stone disease.

Urinary excretion of oxalate, calcium and urate has been investigated in 88 patients affected by idiopathic calcium oxalate stone disease and in 20 normal subjects. Of these ions, only oxalate was found significantly higher in stone formers. Defining hyperoxaluria as urinary oxalate excretion greater than 2 SD above normal, 50% of stone-forming people were found to be hyperoxaluric. When stone formers were classified in normo- and hyperoxaluric, the prevalence of hypercalciuria, hyperuricuria, family history of stone disease and recurrencies in stone formation was the same in both groups. It is concluded that hyperoxaluria is a frequent finding in finding in idiopathic calcium oxalate renal stone disease.

Adult↗