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Biomedical subjects

B Baggio

Publications and source records attributed to B Baggio.

At least 91 records · Page 5Linked to original sources
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↗
PubMed1984

[Abnormalities in the erythrocyte membrane transport of oxalate in calcium oxalate lithogenesis].

The high incidence of a family history and the observation of abnormally high intestinal absorption and urinary excretion of oxalate suggest to consider idiopathic calcium oxalate nephrolithiasis as a metabolic disease characterized by a disorder in oxalate transport. To test this hypothesis, the flux of 14C Oxalate through the membrane of red blood cells was investigated in 24 calcium oxalate stone formers; 18 of the 24 "idiopathic" calcium oxalate stone formers showed an increased oxalate self exchange (75%). Our data seem to support the possibility that "idiopathic" calcium oxalate nephrolithiasis may be considered as a metabolic disease marked by a defect in transmembrane transport of oxalate.

Adult↗
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↗
PubMed1983

Urinary excretion of prostaglandins (PGE2 and PGF2 alpha) and kallikrein in acute glomerulonephritis.

We studied prostaglandins and kallikrein urinary excretion in 14 children with acute poststreptococcal glomerulonephritis within 48 hours of hospital admission (period A), and again, 4-6 weeks later, when they were clinically recovered (period B). Seventeen apparently healthy children were studied as controls. The results (mean +/- SEM) indicate that PGE2 urinary excretion (ng/kg/day) was diminished during both periods of study (control group = 2.06 +/- 0.43, patients = period A 0.91 +/- 0.28 [P less than 0.02], period B 0.92 +/- 0.21 [P less than 0.02]). PGF2 alpha urinary excretion (ng/kg/day) was also suppressed during period A, but not during period B when large individual variability existed (control group = 7.10 +/- 1.07, patients period A 3.56 +/- 0.66 [P less than 0.001], period B 10.51 +/- 5.01 [NS]). Kallikrein urinary excretion (EU/kg/day) was also depressed during the acute phase and remained low during convalescence (control group = 0.492 +/- 0.1, patients period A 0.143 +/- 0.044 [P less than 0.001], period B 0.265 +/- 0.093 [P less than 0.02]). There was no difference in PGE/PGF ratio between controls and patients in the periods of study (control 0.328 +/- 0.055, period A 0.395 +/- 0.144, period B 0.384 +/- 0.128). Urine volume (ml/day) was lower in period A (582 +/- 75.8) but comparable in period B (1020 +/- 140.2) and control children (1210 +/- 80.2). No correlation could be found between the urinary excretion of PGE2, PGF2 alpha and kallikrein with any of the following parameters: urinary or serum sodium and potassium, serum or urinary osmolality, Cosm, urine flow, plasma renin activity, plasma or urinary aldosterone, hypertension or fluid retention.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1982

Calcium oxalate nephrolithiasis: an easy way to detect an imbalance between promoting and inhibiting factors.

Calcium oxalate stone formation depends on both urine oversaturation with calcium oxalate--which in turn depends mainly on oxalate excretion--and the excretion of inhibitors; the possibility that a ratio of these variables might differentiate stone-formers from stone-free subjects was explored, 24-h urine samples from 20 control subjects and 53 idiopathic calcium oxalate stone-formers receiving a standard diet were studied. A further group of 2-h urine samples (from 7 to 9 a.m.). collected after a overnight fast from 16 non-stone and 24 stone-forming persons on a normal diet, were also examined. The ratio 'oxalate/citrate X acid mucopolysaccharides; (Ox/Cit X AMPs) seems capable of differentiating more than 80% of stone-formers from non-stone-formers using both 24- and 2-h urine collection.

Adult↗
PubMed1981

Increased urine angiotensin I converting enzyme activity in patients with upper urinary tract infection.

Angiotensin converting enzyme (ACE) is present within the brush border of the tubular cell of the kidney. Since it has a high molecular mass, ACE activity of urine most probably derives only from tubular cells, thus suggesting the potential usefulness of ACE determination as an index of tubular damage. When assayed with the method described, ACE is optimally active at pH 8 with a calcium concentration exceeding 0.75 mmol/l urine, and is chloride independent. Urine dialysis has no effect on ACE activity. ACE is stable at 4 degrees C for 10 days, but it is inactivated by repeated thawing and freezing. The presence of leucocytes and bacteria does not interfere with the assay. Urine ACE activity was evaluated in patients with upper and lower urinary tract infection, nephrolithiasis, chronic glomerulonephritis and essential hypertension and was found to be significantly increased only in patients affected by upper urinary tract infection and nephrolithiasis.

Calcium↗
PubMed1980

DOCA administration increases renal phospholipase activity in the rat.

The phospholipase activity of renal tissue has been evaluated in controls and in DOCA treated rats. DOCA treated animal showed a higher than normal enzyme activity. Since a phospholipase is the key step in prostaglandin biosynthesis, it is suggested that the increased prostaglandin release promoted by mineraloactive steroids is mediated by an activation of this key enzyme.

Animals↗
PubMed1980

Effects of digoxin on plasma renin activity in hypertensive patients.

The effects of digoxin have been studied on PRA of 11 hypertensive patients treated with a single oral administration of the glycoside or submitted to a prolonged treatment. The experiments performed with a single oral administration (0,5 mg) showed that digoxin induces a significant decrease of the hyperreninemic response induced by furosemide. This effect of digoxin develops very quickly and is well evident when plasma levels of the glycoside are still low. However, in the patients pretreated with a beta blocker, digoxin was completely ineffective in preventing the response to furosemide. In view of the results, the hypothesis is put forward that digoxin mainly acts at renal level through an antiadrenergic activity.

Adult↗
PubMed1979

Kidney kallikrein and phospholipase activities in Milan spontaneously hypertensive rats.

Renal kallikrein and phospholipase activities were evaluated in a strain of spontaneously hypertensive rats developed by Dr. Bianchi in Milan (MHR). MHR showed lower than normal kallikrein and phospholipase activities before, at 3 weeks of age and following the development of hypertension. Kallikrein and phospholipase activities were directly correlated both in normotensive and spontenously hypertensive rats. The data suggest that MHR have a genetic defect in kallikrein and phospholipase activities, which may play a pathogenetic role in the development of high blood pressure.

Animals↗
PubMed1978

In vivo activation of renal phospholipase activity by bradykinin in the rat.

Activation of a renal acylhydrolase by bradykinin (BK) with subsequent release of prostaglandins precursor arachidonic acid has been postulated but not yet demonstrated. BK was infused into the left artery of 27 rats which were subdivided into 9 groups according to BK concentration (10, 100 and 1000 ng/min) and time of infusion (20, 40 and 60 min). The rats were then sacrificed and the left to right ratio of renal phospholipase activity was determined. The data obtained were processed by a factorial analysis of variance which allowed the effect of BK and the time of infusion to be evaluated independently as well as interdependently. The results of the statistical analysis showed that phospholipase activity depends on both BK dosage and infusion time and that there is no interaction between dose and time. These findings offer evidence for the "in vivo" activation of the kidney phospholipase activity by BK.

Animals↗
PubMed1978

Antibody-coated bacteria in the urinary sediment of rats with experimental pyelonephritis.

The appearance of antibody-coated bacteria in urinary sediment has been evaluated in rats with experimental pyelonephritis. At day 7 after induction of pyelonephritis, 9 out of 11 rats demonstrated antibody-coated bacteria in the urinary sediment. The other 2 rats never had a positive urinary sediment. Following removal of the pyelonephritic kidneys, antibody-coated bacteria disappeared in 7 of 9 previously positive rats. In the 2 rats which continued to show antibody-coated bacteria, the infecting organisms were found in the remaining kidney. The 2 rats which never developed antibody-coated bacteria in urinary sediment had a higher then normal serum antibody titer, and 1 rat with antibody-coated bacteria showed a normal serum antibody titer. It is concluded that although the search for antibody-coated bacteria in urinary sediment is a very useful technique, its negativity does not exclude upper urinary tract involvement; in the case of renal parenchymal infection, immunity is not the same at the systemic and the local site.

Animals↗
PubMed1977

Fructose-induced hyperuricemia in essential hypertension.

A rapid intravenous fructose load was given to nine normouricemic essential hypertensive and eight control subjects. The following increase in plasma uric acid concentration was significantly higher in hypertensives than in controls. There was no significant difference in urinary excretion of urate between the two groups. Since the increase in uric acid concentration brought about by fructose is most probably due to an increased metabolism of preformed purine nucleotides, it is suggested that essential hypertensive patients have a higher than normal "pool" of purine nucleotides.

Adult↗
PubMed1977

[Epidemiological studies of blood levels of cholesterol and triglycerides in a school-age population of Veneto].

During the school year 1974-75 serum cholesterol has been evaluated in the whole school population (520 subjects, 268 males and 252 females, age ranging from 6 to 14 years) of Saccolongo, a village which is about 20 kilometers from Padova (Italy) and serum triglycerides have been further evaluated in a random population of 161 subjects (90 males and 71 females, age ranging from 6 to 11 years). Serum cholesterol values did not show any significant difference between males and females. Analysis of serum cholesterol in the various age groups revealed that it was significantly higher in females at age 6 (t = 2.2296; p less than 0.05). A significant reduction in serum cholesterol values has been found at age 11 both in males (t = 4.7810; p less than 0.001) and in females (t = 5.6134; p less than 0.001). Serum cholesterol and triglycerides values did not correlate (r = 0.404). Serum triglycerides were higher in girls than in boys (t = 2.1360; p less than 0.05). Analysis of the serum triglycerides values in the various age groups were constant in males (F = 0.4161) and inconstant in females (F = 3.8844; p less than 0.01) where age groups 8 (t = 3.5127; p less than 0.005) and 11 (t = 3.5238; p less than 0.005) showed higher than normal values.

Age Factors↗