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Biomedical subjects

S Favaro

Publications and source records attributed to S Favaro.

At least 55 records · Page 3Linked to original sources
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↗
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↗
PubMed1975

A possible role of the kidney in activating a renin preinhibitor.

In order to verify the possibility than human plasma and kidney can activate a renin preinhibitor (Phospholipid) into inhibitor (lysophospholipid), constant quantities of preinhibitor were added to plasma and kidney homogenate. Addition of preinhibitor to plasma did not modify the quantity of Angiotensin I that developed. On the other hand, addition of preinhibitor to crude kidney homogenate, followed by incubation with human angiotensinogen, caused a significant fall in the quantity of Angiotensin I generated. While plasma is deficient in the specific enzyme delegated to the transformation of preinhibitor into inhibitor, it appears that this enzyme is present in the kidney.

Angiotensin II↗
PubMed1975

Effect of uninephrectomy on tissue kallicrein concentration of the remaining kidney.

Compensatory renal hypertrophy has been induced in rats by uninephrectomy. Tissue kallicrein concentration of the remaining kidney was evaluated 5, 10, 15 and 20 days after operation. The previously removed kidneys were used as controls. In the hypertrophic kidney the kallicrein increases progressively up to 20 days after uninephrectomy. Since kallicrein generates kinins, potent vasodilators, it is suggested that the increase in renal blood flow observed after uninephrectomy might be promoted by an overproduction of kinins.

Animals↗
PubMed1975

Renal kallikrein content of spontaneously hypertensive rats.

1. The kallikrein content of kidneys from spontaneously hypertensive and normal rats at birth and at age 37 days was determined. 2. Kallikrein values were significantly lower in the hypertensive rats. 3. It is suggested that the lowered kallikrein may be related to the development of hypertension.

Aging↗