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Biomedical subjects

B Baggio

Publications and source records attributed to B Baggio.

At least 55 records · Page 3Linked to original sources
PubMed1993

Evidence of a link between erythrocyte band 3 phosphorylation and anion transport in patients with 'idiopathic' calcium oxalate nephrolithiasis.

This study was carried out to verify the hypothesis of a link between faster endogenous phosphorylation of band 3 protein, the anion carrier, and anomalous oxalate transmembrane self-exchange found in erythrocyte from calcium oxalate renal stone formers. Agents able to modify 32P-labelling of band 3 protein induced a concurrent modification in oxalate transmembrane flux. Cyclic AMP- and phospholipid-sensitive Ca(2+)-independent protein kinases seem to be critical modulators of band 3 function. These observations demonstrate a close link between the band 3 phosphorylation state and its anion transport function, and provide new insights into the pathogenetic mechanisms of the cellular anomalies observed in calcium-oxalate renal stone disease.

Anion Exchange Protein 1, Erythrocyte↗
PubMed1992

Tyrosine-protein kinase inhibition in human erythrocytes by polyphosphoinositides (PIP and PIP2).

In human erythrocytes Ser/Thr- and Tyr-phosphorylations of cytoplasmic domain of band 3 are catalyzed by casein kinase I and Tyr-protein kinase respectively, both distributed between cytosol and membrane structures. The results reported here show that purified cytosolic Tyr-protein kinase activity, assayed on added substrates such as poly(Glu,Tyr)4:1 and isolated chymotryptic fragments of band 3 cytoplasmic domain (cdb3), is potently inhibited by PIP and even more by PIP2. Similar inhibitory effects are displayed by these polyphosphoinositides also on the endogenous Tyr-phosphorylation of band 3, when they are added to the isolated native membranes, thus suggesting their involvement in regulating in-vivo Tyr-phosphorylation of membrane proteins.

Adenosine Triphosphate↗
PubMed1992

Glycosaminoglycans prevent morphological renal alterations and albuminuria in diabetic rats.

Abnormal glycosaminoglycan metabolism is involved in the onset of anatomo-functional derangements in diabetic nephropathy, and determines the loss of glomerular basement membrane anionic charges leading to albuminuria. Glycosaminoglycan administration was shown to increase the negative electrical potential of the vessel wall, inhibit mesangial cell proliferation, which is an anatomical hallmark of diabetic nephropathy, and slow down the progression to uremia in subtotally nephrectomized rats, a model that shares some pathogenetic key events with diabetic nephropathy. Based on these considerations, we verified the effect of exogenous glycosaminoglycans on renal involvement in streptozotocin diabetic rats. Long-term administration of two glycosaminoglycans (low-molecular weight heparin and dermatan sulphate) prevented glomerular basement membrane thickening, glomerular anionic charge reduction, as well as the onset of albuminuria without affecting glomerular filtration rate and metabolic control of the disease. Our data demonstrate that the long-term administration of glycosaminoglycans has a favorable effect on morphological and functional renal abnormalities in diabetic rats.

Albuminuria↗
PubMed1992

Idiopathic calcium oxalate nephrolithiasis: a cellular disease.

Physico-chemical, metabolic and hormonal theories regarding the pathogenesis of calcium oxalate nephrolithiasis do not sufficiently explain many features of this disease. The recent findings of an abnormally faster oxalate self-exchange and higher phosphorylation of band 3 in erythrocytes of idiopathic calcium oxalate stone formers suggest the hypothesis that nephrolithiasis may be a cellular disease, characterized by a defect in the function of the anion-exchange. The cellular anomaly seems genetically controlled. Band 3 anion exchanger function seems to be biochemically regulated through modulation of band 3 phosphorylation, which depends on cyclic AMP- and phospholipid-sensitive Ca2+ independent protein kinases. In this light, a reduced glycosaminoglycan concentration in the erythrocyte membranes of stone formers might play a role, as these molecules exert a strong inhibitory effects on band 3 phosphorylation and anion transport in vitro and in vivo. An in vivo trial was performed in which stone formers were administered glycosaminoglycans orally. A reduction in oxalate excretion, and oxalate renal clearance, and a simultaneous correction of the abnormal RBC oxalate flux and band 3 phosphorylation were observed. These data suggest the existence of a link between the erythrocyte abnormality and oxalate transport by the kidney and gut.

Animals↗
PubMed1991

Correction of erythrocyte abnormalities in idiopathic calcium-oxalate nephrolithiasis and reduction of urinary oxalate by oral glycosaminoglycans.

Calcium-oxalate nephrolithiasis is associated with a defect in erythrocyte oxalate self-exchange and an abnormal rate of erythrocyte membrane protein phosphorylation. There is evidence that glycosaminoglycans (GAGs) have a regulatory effect on both of these processes. This study tested the hypothesis that modifications of erythrocyte oxalate self-exchange induced by oral GAGs are paralleled by similar changes in overall oxalate metabolism. 40 patients with idiopathic calcium-oxalate nephrolithiasis were treated for 15 days with 60 mg/day of a mixture of GAGs. By day 15 of treatment there were significant reductions from baseline in erythrocyte oxalate self-exchange (mean [SD] 1.67 [1.18] vs 2.59 [1.63] x 10(2) per min; p less than 0.005) and erythrocyte membrane protein phosphorylation (55.8 [7.3] vs 72.9 [6.8] x 10(-3) cpm/mg protein; p less than 0.005), but also in urinary oxalate excretion (0.24 [0.09] vs 0.31 [0.15] mmol/24 h; p less than 0.005). This finding suggests similar changes in both erythrocytes and other cells more important in oxalate handling. The changes had reversed by 15 days after withdrawal of treatment. Acute intravenous administration of GAGs (60 mg) induced a fall in carbon-14-labelled oxalate renal clearance (143 [13] vs 169 [28] ml/min; p less than 0.005), which strongly suggests the participation of the kidney. However, reduced oxalate absorption from the intestine, and even decreased synthesis of oxalate, cannot be ruled out.

Administration, Oral↗
PubMed1991

Effects of the oral administration of glycosaminoglycans on cellular abnormalities associated with idiopathic calcium oxalate nephrolithiasis.

Oral administration of mixture of extractive glycosaminoglycans to a group of renal stone formers led to a significant decrease in oxalate self-exchange and in erythrocytes membrane protein phosphorylation traits that are abnormal in the majority of patients with idiopathic calcium nephrolithiasis. The action of glycosaminoglycans at the cellular level is probably due to their modulating activity on certain membrane protein kinases. The proven effect of the glycosaminoglycans opens a new pharmacological approach to the prevention of recurrent nephrolithiasis.

Administration, Oral↗
PubMed1990

Is hydrochlorothiazide-induced hypocalciuria due to inhibition of prostaglandin E2 synthesis?

1. Since prostaglandin E2 could play a role in idiopathic hypercalciuria, and considering the well-established hypocalciuric action of hydrochlorothiazide, we have evaluated the effect of 15 days' treatment with hydrochlorothiazide in 10 hypercalciuric male stoneformers on urinary Ca2+ and prostaglandin E2, as well as on plasma bicyclo-prostaglandin E2, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and parathyroid hormone. 2. In addition to lowering urinary Ca2+ (P less than 0.001), hydrochlorothiazide also promoted a significant fall in urinary prostaglandin E2 (P less than 0.001), plasma bicyclo-prostaglandin E2 (P less than 0.001) and 1,25-dihydroxyvitamin D (P less than 0.01), and an increase in plasma parathyroid hormone (P less than 0.025), whereas plasma 25-hydroxyvitamin D was unchanged. 3. A positive correlation between urinary Ca2+ and prostaglandin E2 was present before (P less than 0.00005), but not after, hydrochlorothiazide. Plasma bicyclo-prostaglandin E2 and plasma 1,25-dihydroxyvitamin D were positively correlated both before (P less than 0.005) and after (P less than 0.005) hydrochlorothiazide, as was also the percentage change in each induced by the drug (P less than 0.05). Furthermore, the changes in plasma 25-hydroxyvitamin D and plasma 1,25-dihydroxyvitamin D after hydrochlorothiazide were negatively correlated (P less than 0.05). 4. It is suggested that a block of prostaglandin E2 synthesis plays a role in the effect of hydrochlorothiazide on Ca2+ metabolism, most probably through an inhibition of 1 alpha-hydroxylase activity.

Adult↗
PubMed1990

Glycosaminoglycan content, oxalate self-exchange and protein phosphorylation in erythrocytes of patients with 'idiopathic' calcium oxalate nephrolithiasis.

1. This study was performed to test the hypothesis that glycosaminoglycans may play an important role in the observed abnormalities in oxalate flux seen in patients with calcium oxalate nephrolithiasis. 2. Oxalate flux rate, erythrocyte membrane glycosaminoglycan content, membrane protein phosphorylation and effect of heparan sulphate on erythrocyte oxalate flux in vitro were studied in control subjects and patients with calcium oxalate nephrolithiasis. 3. In comparison with control subjects, renal stone-formers showed a significantly higher oxalate self-exchange, a lower erythrocyte membrane glycosaminoglycan content and a higher membrane phosphorylation rate. In stone-formers, erythrocyte glycosaminoglycan content correlated inversely with both oxalate flux rate and protein phosphorylation. In vitro, heparan sulphate promoted a significant fall in the rate of oxalate self-exchange. 4. These findings support the hypothesis that a lower erythrocyte membrane content of glycosaminoglycans enhances membrane protein phosphorylation, leading to an increased rate of transmembrane oxalate flux.

Adult↗
PubMed1990

Very early nutrition supplementation in burned patients.

We studied some metabolic and hormonal effects of a very early nutrition supplementation in burned patients. The patients were divided into two groups of 10 patients each. Supplementation in the first group, the very early nutritionally supplemented (VENS) group, was started immediately after admission, ie, after 4.4 +/- 0.5 h (mean +/- SEM) from the injury; it was started after 57.7 +/- 2.6 h from the injury in the second group (control group). Hormonal and metabolic indices were recorded every 4 d up to 28 d. In the VENS group, the nitrogen balance became positive in 8.8 +/- 4.1 d whereas it took 24.1 +/- 6.9 d in the control group (p less than 0.05). Urinary catecholamine excretion and plasma glucagon concentrations were lower during the first 2 wk of observation in the VENS group compared with the control group. Insulin concentrations were significantly higher on the fourth and eighth days in VENS patients and plasma cortisol concentrations were similar in both groups.

Adult↗
PubMed1989

High urinary excretion of glycosaminoglycans: a possible marker of glomerular involvement in diabetes.

Many insulin-dependent diabetic patients with albuminuria in the "not at risk range" for diabetic nephropathy present high urinary excretion rates of glycosaminoglycans. A lysine provocative test in these subjects disclosed abnormal urinary excretion of albumin, unlike findings obtained in insulin-dependent diabetic patients with normal urinary excretion rates of glycosaminoglycans. These data support the hypothesis that high urinary excretion of glycosaminoglycans is a marker of glomerular involvement in diabetes mellitus.

Adult↗
PubMed1989

Specific features of left ventricular hypertrophy in hypertensive obese women. An echocardiographic study.

The echocardiographic features of the left ventricle of 37 obese women (body mass index above 30) and 37 lean controls, matched for sex, age, height and blood pressure levels, were studied. Twenty-six patients in each group were hypertensive. The normotensive obese patients did not show any differences, comparing to the normotensive controls; on the contrary, the hypertensive obese patients had higher left ventricular mass (LVM), stroke volume and cardiac output (CO), and lower total peripheral resistance (TPR) than the hypertensive controls. A positive correlation was found between the LVM and the CO (r = 0.57, P less than 0.01) in hypertensive obese patients, and between the relative wall thickenss (h/r, that is the ratio between the left ventricular wall thickness and the left ventricular radius) and TPR (r = 0.64, P less than 0.01) in the hypertensive controls. It is concluded that obesity per se does not determine left ventricular hypertrophy in women; however, when obesity is associated with arterial hypertension, a distinct pattern of hypertrophy, characterized by high CO and low TPR, develops.

Adult↗
PubMed1988

Effects of imidazole-2-hydroxibenzoate on glycosaminoglycan and albumin urinary excretion in type 1 diabetic patients.

The effect of imidazole-2-hydroxibenzoate on urinary excretion rates of glycosaminoglycans and albumin in 22 insulin-dependent diabetics with albumin excretion rates under 300 mg/day was evaluated in a 165-day double blind crossover study. Unlike placebo, the drug reduced glycosaminoglycan and albumin excretion rates significantly after 40 and 60 days of treatment, and the effects were significantly intercorrelated. Moreover, a parallel reduction in urinary excretion of N-acetyl-beta-D-glucosaminidase was also observed. These pharmacological effects may have a positive impact on the subsequent natural history of diabetic nephropathy.

Acetylglucosaminidase↗