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Biomedical subjects

G Sanna

Publications and source records attributed to G Sanna.

At least 91 records · Page 5Linked to original sources
PubMed1982

In-vivo activation of circulating inactive renin by the ischemic kidney in man.

The role of the kidney as a possible source or as activator of inactive renin was studied in 22 patients with Essential Hypertension (EH) and in 20 patients with Unilateral Renal Artery Stenosis (RAS). Active and inactive renin (trypsin activation) were measured in blood samples taken simultaneously from both renal veins and from a peripheral artery during acute diuretic stimulation induced by furosemide 40 mg i.v. In EH pts active and trypsin-activated renin were significantly higher in both renal veins than in arterial blood (P less than 0.001 and P less than 0.02 respectively) whereas no difference was seen as far as inactive renin is concerned. In unilateral RAS trypsin-activated and active renin from the ischemic kidney were significantly higher (P less than 0.01 and P less than 0.005 respectively) while inactive renin was significantly lower (P less than 0.005) than in arterial blood. No significant difference was seen between arterial and renal venous blood from the contralateral kidney as far as active and inactive renin are concerned. When comparing the V-A differences for active renin to the corresponding V-A differences for inactive renin from the ischemic kidney a significant negative correlation appeared (r = -0.49 p less than 0.05) whereas no correlation was found from the contralateral kidney (r = -0.26 n.s.). These data demonstrate that the ischemic kidney, in addition to its ability to release active renin, can also activate circulating inactive renin.

Adult↗
PubMed1982

Plasma active and inactive renin and urinary kallikrein in normal subjects in response to hydrochlorothiazide, spironolactone or aldosterone administration.

The aim of this study has been to see whether acute variations in the proportions of circulating active and inactive renin in normal subjects were related to concurrent changes in the excretion of urinary kallikrein. Hydrochlorothiazide (50 mg/day) was given to 6 normal volunteers for 6 days; another group of 6 normal subjects received spironolactone (300 mg/day) for 6 days whereas synthetic aldosterone (0.5 mg/day) was administered i.m. for three days to 3 normal subjects. Both diuretics induced a sharp rise in active and total renin and a significant transient decrease in inactive renin so that the active: total renin proportion significantly increased. Urinary kallikrein excretion did not significantly change in either group. Parenteral administration of aldosterone induced a striking fall in all renin components without changing the proportions of active and inactive renin whereas urinary kallikrein excretion increased. These results indicate that changes in active: total renin proportions can occur without parallel variations in urinary kallikrein excretion. The latter cannot be used, therefore, as a reliable index of the possible role of renal kallikrein as activator in-vivo of inactive renin in man.

Adult↗
PubMed1981

Iron overload and desferrioxamine chelation therapy in beta-thalassemia intermedia.

This study on serum ferritin levels in urinary iron excretion after 12h subcutaneous infusion of desferrioxamine in 10 thalassemia intermedia patients shows that even nontransfusion-dependent patients may have positive iron balance resulting in iron overload from 5 years of age. However, the iron overload found in these patients appears to be much lower than in age matched patients with transfusion-dependent thalassemia major. Iron overload increases with advancing age, as shown by increasing serum ferritin levels and desferrioxamine-induced urinary iron elimination. After a six month trial of 12h continuous subcutaneous desferrioxamine administration there was a significant decline in serum ferritin levels. From this study it seems that iron chelation is indicated in thalassemia intermedia patients over 5 years of age in order to prevent iron accumulation. However, the appropriate treatment schedule should be tailored to the individual needs of each patients, established by close monitoring of serum ferritin levels and desferrioxamine-induced urinary iron elimination.

Adolescent↗
PubMed1981

Optimum tryptic activation of inactive renin in human plasma is independent of endogenous anti-tryptic activity.

1. Plasma samples from 31 normal subjects were treated (at 4 degrees C, pH 7.0, for 2 min) with different concentrations of trypsin (500, 1000, 2000, 3000 and 4000 microgram/ml) in order to assess which concentration yielded the maximum activation of inactive renin. 2. Endogenous antitryptic activity was also measured in all samples; the mean value +/- SD (in microgram of trypsin inhibited by 1 ml of plasma) was 953 +/- 550 microgram/ml (range 34-1800 microgram/ml). 3. In the entire group of subjects the values of trypsin-activated renin measured with trypsin at 2000 microgram/ml were significantly higher than those obtained with lower or higher trypsin concentrations. 4. With subjects divided into subgroups according to their endogenous anti-tryptic activity, the maximum yield of activation was reached with trypsin at 2000 microgram/ml. 5. No significant correlations were found between single values of active, inactive or trypsin-activated renin and the corresponding levels of endogenous anti-tryptic activity. However, a weak but significant correlation (r = 0.39, P less than 0.05) was found between single values of anti-tryptic activity and the corresponding percentage of activation of inactive renin. 6. Thus the maximum activation of inactive renin at 4 degrees C for 2 min is obtained with trypsin at 2000 microgram/ml independently of the corresponding endogenous anti-tryptic activity. It is not excluded that the content of protease inhibitors in human plasma might affect the proportion in vivo of circulating active and inactive renin.

Adult↗
PubMed1981

Chronic liver disease in transfusion-dependent thalassemia: liver iron quantitation and distribution.

The quantitative and/or qualitative distribution of liver iron was assessed in 81 transfusion-dependent thalassemia major patients with chronic liver disease (36 with chronic active hepatitis, 23 with chronic persistent hepatitis, 22 with siderosis). Viral marker studies showed only 3 cases with both HBsAg and anti-HBc positivity in the serum, while the others had anti-HBc and anti-HBs or only anti-HBs or no B viral markers. A significantly higher iron overload was found in chronic hepatitis, particularly chronic active hepatitis, than in siderosis. The increased iron overload may be due to less intensive chelation treatment, higher intestinal absorption secondary to lower mean Hb levels, and/or to liver inflammation-dependent iron deposition. The liver iron overload in turn amy facilitate the development or persistence of chronic progressive liver disease.

Adolescent↗
PubMed1981

Glucose-6-phosphate dehydrogenase red blood cell phenotype in GdMediterranean heterozygous females and hemizygous males at birth.

The distribution of red blood cell G6PD phenotype was studied by means of the methemoglobin elution test in newborn (46) and adult (50) GdMediterranean heterozygous females and newborn (20) and adult (30) hemizygous males. Newborn heterozygotes had a statistically significant (P less than 0.0005) lower mean red blood cell G6PD enzymatic activity (3.23 +/- 1.04) than did normal newborns (8.78 +/- 1.91), whereas there was no significant difference (P greater than 0.30) from the mean of adult heterozygotes (2.93 +/- 0.86). Like adults, newborn heterozygous females showed: (1) a clear correlation (P less than 0.001) between the percentage of enzyme-deficient red blood cells and G6PD enzymatic activity; and (2) the expected two red blood cell population, i.e., one deficient and the other normal (mosaicism). However, in newborns, the distribution of the subjects according to G6PD-deficient red blood cell percentage (mean percent, 43.67) was significantly shifted (P less than 0.025) in favour of the normal phenotype, unlike adult heterozygotes, who showed a symmetrical distribution of G6PD positive and negative red blood cells (mean percent G6PD-deficient red blood cells, 53.27; P greater than 0.20). Newborn hemizygous males showed a consistent percentage (average, 8.28 +/- 2.2) of stained red blood cells due to the presence of young erythrocytes (pseudomosaicism) unlike the occasional stained cells (less than or equal to 5) seen in adults. The prevalence of hyperbilirubinemia in hemizygous males and heterozygous females was 10.22 and 2.2%, respectively, whereas in G6PD normal newborns it was 5.1%. The practical implication of this study is that the diagnosis at birth of the heterozygous state for G6PD deficiency of the Mediterranean type may be more difficult than in adults. Therefore, very sensitive methods, such as the methemoglobin elution test, should be carried out.

Erythrocytes↗
PubMed1981

[Role of renin profile and age in the choice of the therapeutic approach of arterial hypertension (author's transl)].

A group of 116 patients with grade I-II (W.H.O.) essential hypertension was studied. A diuretic treatment was instituted as a first step of therapy in 50 patients while the remaining 66 were firstly treated with beta-blockers. After 6 weeks of treatment the drugs were combined in those patients who did not achieve blood pressure control; this combination therapy was again maintained for 6 weeks and, if necessary, a vasodilating agent was added thereafter. The results show that with diuretic treatment alone diastolic blood pressure was brought to normal values (less than 95 mmHg) in 3/4 of our low renin patients, in 2/3 of normal renin and in 1/3 of high renin hypertensives. On the contrary among the group of patients treated with a beta-blocker alone more than half of the high and normal renin patients were controlled whereas this goal was achieved in only 1/4 of the low renin patients. Similar behaviour was observed subdividing the subjects in young (less than 35 yrs), middle-aged (36-49 yrs) and older (greater than 50 yrs) patients. In conclusion our data indicate that age must be taken into account in classifying hypertensive patients in renin subgroups. In addition if a renin-sodium profile is available, it can be useful in choosing between diuretics or beta-blocker as a first step treatment. Alternatively, younger patients are more likely to have better hypotensive responses with beta-blockers whereas in older patients antihypertensive treatment should preferentially be started with diuretics alone.

Adrenergic beta-Antagonists↗
PubMed1980

Interaction between the glucose-6-phosphate dehydrogenase deficiency and thalassaemia genes at phenotype level.

No significant differences were observed in the mean values of Hb A2 levels and red cell indices between G6PD- and G6PD+ beta thalassaemia carriers apart from the MCV, which was significantly higher in beta thalassaemia G6PD- subjects, but still in the thalassaemia carrier range. No difference was seen between G6PD+ and G6PD- alpha thalassaemia carriers. G6PD+ beta thalassaemia carriers show a significant increase in G6PD levels expressed as activity per g of Hb and to lesser extent as activity per number of red cells x 10(9); in G6PD+ alpha thalassaemia carriers this increase is statistically significant only when the enzyme levels are expressed as activity per g of Hb. G6PD- beta thalassaemia carriers had enzyme levels higher than non-thalassaemic G6PD- subjects only when the activity is expressed per g of Hb. G6PD activity was found to be increased in G6PD+ and G6PD- Hb H disease patients.

Erythrocyte Count↗
PubMed1980

Serum ferritin, liver iron stores, and liver histology in children with thalassaemia.

Serum ferritin, liver iron stores, and liver histology were studied in 38 children with thalassaemia major who were being treated by regular blood transfusions. There was no correlation between serum ferritin levels and either the number of transfusions or the amount of iron deposited in the liver. However, for a given level of iron stores, ferritin levels were higher in patients with chronic hepatitis (including chronic aggressive and chronic persistent forms) than in those with hepatic siderosis only. We conclude that serum ferritin reflects tissue iron deposits in regularly transfused thalassaemic patients, only in the absence of hepatitis.

Blood Transfusion↗
PubMed1980

Chronic liver disease in transfusion-dependent thalassaemia: hepatitis B virus marker studies.

The systematic screening of 253 children with transfusion-dependent homozygous beta-thalassaemia revealed a high incidence of hepatitis B virus markers. The highest frequencies of hepatitis B surface antigen (HBsAg) and antibody to hepatitis B core antigen (anti-HBc) were found in the group of patients with the smallest number of transfusions, while the highest frequency of antibody to hepatitis B surface antigen (anti-HBs) was detected in the patients who had had the largest number of transfusions. Follow-up of these patients showed (a) a high incidence of acute hepatitis B, which was mainly subclinical; (b) normal hepatitis B surface antigen clearance and normal antibody to hepatitis B surface development; and (c) a high frequency of increased transaminase values for over six months. In all the subjects with persistently high transaminase, histological examination revealed chronic persistent hepatitis or chronic active hepatitis. Apart from two cases of chronic active hepatitis with no B virus markers, and two cases of chronic persistent hepatitis with HBsAg and anti-HBc in the serum, all these subjects were anti-HBs positive but HGsAg and anti-HBc negative.

Adolescent↗