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Biomedical subjects

G Barsotti

Publications and source records attributed to G Barsotti.

At least 91 records · Page 5Linked to original sources
PubMed1986

Effects of a low phosphorus, low nitrogen diet supplemented with essential amino acids and ketoanalogues on serum triglycerides of chronic uremic patients.

The effects were studied of a vegetarian low-protein, low-phosphorus diet supplemented with essential amino acids and ketoanalogues and those of maintenance hemodialysis (MHD) and free diet on the serum triglycerides (STG) of 85 patients with chronic renal failure. Following dietary therapy STG decreased significantly in the 61 male patients (from 185.7 +/- 89.8 to 153.5 +/- 68.7 mg/dl; p less than 0.001), whereas in the females the decrease was not significant (from 189.1 +/- 83.9 to 167.0 +/- 62.2 mg/dl; NS). When patients changed to MHD therapy and free diet STG increased again. We can conclude that the correction of hypogonadism of chronic male uremics largely accounts for the improvement of hypertriglyceridemia, though other factors are likely to contribute.

Adult↗
PubMed1986

The role of metabolic acidosis in causing uremic hyperphosphatemia.

Metabolic acidosis was corrected within 1 h in 7 chronic anuric uremic patients on maintenance hemodialysis and, in the course of a week, in 11 other patients on conservative therapy. These patients were on a diet supplying constant amounts of phosphate throughout the duration of the study. In the former group the intravenous infusion of sodium bicarbonate was used, and, in the latter, the oral administration of sodium citrate. In both groups serum phosphate was found to decrease significantly. In the patients on conservative therapy, phosphaturia also had significantly decreased while no changes occurred in their daily fecal loss of phosphate that was measured in 3 patients. These findings indicate that metabolic acidosis is one of the causes of hyperphosphatemia in chronic uremic patients.

Acidosis↗
PubMed1986

Parathyroid function and pituitary-gonadal axis in male uremics; effects of dietary treatment and of maintenance hemodialysis.

Parathyroid and pituitary-gonadal secretions were studied in 18 male uremics following a low protein diet supplemented with essential amino acids and ketoanalogues (SD), and in 8 subjects on maintenance hemodialysis (MHD). SD corrected high serum PTH and low serum testosterone (sT) levels, while pituitary hormones (LH, FSH, PRL) were elevated and did not change. Patients on MHD had very high siPTH, PRL and LH levels, while sT was markedly low. These data suggest that PTH is a prominent cause of sexual dysfunction in male uremics, since SD can restore sT secretion by correcting PTH levels, without improving pituitary dysfunctions. In dialyzed patients secondary hyperparathyroidism worsens and is an important cause of low sT secretion, but also a severe hyperprolactinemia develops, which may further impair gonadal function.

Adult↗
PubMed1984

Serum oxalic acid in uremia: effect of a low-protein diet supplemented with essential amino acids and ketoanalogues.

Serum oxalic acid (sOx) was determined with a new, specific enzymatic method in 73 uremic patients and the values were plotted against serum creatinine. 41 patients received a free mixed diet, and 32 similar patients were given a low-nitrogen diet supplemented with essential amino acids, ketoanalogues, and calcium carbonate (AD). A significant correlation was found between serum creatinine and sOx levels in patients following a free mixed diet, while no correlation appeared in patients on AD: The sOx concentrations were significantly lower and even normal in this group, and a significant reduction of sOx occurred in 10 patients with chronic renal failure, who changed from a free mixed diet to the AD. The lowering of sOx concentration in patients following AD is attributed both to low intake of its metabolic precursors and to the oral calcium carbonate supplementation.

Amino Acids, Essential↗
PubMed1984

The decline of renal function slowed by very low phosphorus intake in chronic renal patients following a low nitrogen diet.

The rate of progression of renal failure has been evaluated in two homogenous groups of chronic renal patients with early insufficiency. In both groups the diet supplied the same amount of calories (approximately 35 Kcal/kg/day) and the protein intake was equally restricted (approximately, 0.6 g/kg/day); however, in Group 1 the phosphorus intake was lower (6.5 mg/kg/day) than in Group 2 (12 mg/kg/day). In both groups the rate of decline of creatinine clearance decreased when patients changed from a free mixed diet to the specially controlled diets, but in Group 1 (lower phosphorus intake) this change was much more marked than in Group 2. Elevated mean levels of serum phosphate and of urinary output of phosphate per unit of creatinine clearance, and elevated mean levels of serum iPTH were found in the patients of Group 2, whereas Group 1 patients had normal mean levels of serum phosphate and of iPTH, and the phosphaturia per unit of creatinine clearance was almost normal. The role of such abnormalities in urinary and serum phosphate, and of secondary hyperparathyroidism, on the progression of renal failure is discussed.

Adult↗
PubMed1983

Comprehensive study of haemostasis in chronic uraemia.

A comprehensive study of haemostasis has been performed in a homogeneous group of 25 adult patients with conservatively treated chronic uraemia. We have found prolonged bleeding time, impaired platelet adhesiveness and aggregation, and decreased platelet factor 3 activity, increased values of fibrinogen, of factor VIII activity and related antigen, and of combined levels of factors II, VII and X. Non-significantly abnormal concentrations of factor XIII and of plasminogen and significantly lower values of plasminogen activators and higher values of urokinase inhibitors and anti-plasmin have also been found. Fibrinogen degradation products were detected in the urine of some patients.

Adult↗
PubMed1983

Comprehensive study of haemostasis in nephrotic syndrome.

A comprehensive study of haemostasis has been performed in a homogeneous group of 20 patients with nephrotic syndrome without renal failure. We have found unchanged number of platelets and a significant increase of platelet adhesiveness and aggregation; increased levels of activity and related antigen of fibrinogen, of factor VIII, of activity of factors II, VII and X and of antigens of factors XIII. Antithrombin III was unchanged in plasma and was detected in the urine. Euglobulin lysis times were decreased, and levels of plasminogen and its activators were increased after a venous occlusion test. At the same time urokinase inhibitors and antiplasmins were increased not only after, but also before a venous occlusion test. Fibrinogen degradation products have been found in the urine of all our patients but not in their sera.

Adult↗
PubMed1983

Restricted phosphorus and nitrogen intake to slow the progression of chronic renal failure: a controlled trial.

Twenty chronically azotemic patients (experimental group) with a mean creatinine clearance of 22.5 +/- 9.4 ml/min followed a diet supplying daily, per kilogram of body weight, 7.0 mg of phosphorus and 0.5 g of protein, mostly of high biological value, for 11.3 months. A group of 19 similar patients (control group) followed a diet supplying daily, per kilogram of body weight, 12 mg of phosphorus and 0.8 g of protein for a similar period of time. In the experimental group, the serum inorganic phosphorus, urea, and iPTH (both N-terminal and C-terminal fragments) decreased significantly. The creatinine clearance decreased by -0.59 +/- 0.7 ml/min per month prior to the commencement of the experimental diet and increased by a mean of 0.1 +/- 0.4 ml/min per month during the period of study. In the control group, the serum inorganic phosphorus increased, the serum urea and iPTH remained practically constant, and the mean creatinine clearance continued to decrease at a rate not significantly different from that prior to the onset of the study (-0.50 +/- 0.66 and -0.44 +/- 0.10 ml/min per month, respectively). The mechanisms by which the low-phosphorus, low-nitrogen diet slows the progression of renal failure are discussed, and the practical importance of prescribing the dietetic restriction early in the course of renal disease is stressed.

Adult↗
PubMed1983

Serum uric acid in mild essential hypertension.

The mean serum level of urate and the incidence of hyperuricemia have been found to be normal in 85 patients with untreated essential arterial hypertension without renal failure. On the contrary, the incidence of hyperuricemia has been found to be high in 36 similar patients on a low salt diet and in 19 others who received diuretics. Uricemia decreased in 55 patients on a low salt diet who received hydrazinophthalazine (hydralazine) and in 10 other patients who changed their diet from a low salt diet to a diet supplying normal amounts of salt. These results indicate that essential arterial hypertension does not cause hyperuricemia.

Adult↗
PubMed1983

Three years experience with a very low nitrogen diet supplemented with essential amino acids and keto-analogues in the treatment of chronic uraemia.

A low nitrogen, low phosphorus diet, supplemented with essential amino acids and keto-analogues, was administered to 48 chronic uraemics for a maximum of 36 months. In 10 cases renal function deteriorated and dialysis was started; eight patients changed to the dialytic therapy having difficulties in complying to the diet and three died for reasons not directly related to renal failure. The remaining twenty-seven patients are still on dietetic treatment and their renal function has not changed significantly. Their serum inorganic phosphorus and their circulating iPTH decreased significantly. Their subjective and objective conditions are satisfactory and no manifestation of protein malnutrition or other unwanted effects are detectable.

Adult↗
PubMed1981

Effects on renal function of a low-nitrogen diet supplemented with essential amino acids and ketoanalogues and of hemodialysis and free protein supply in patients with chronic renal failure.

Creatinine clearance has been repeatedly measured in three groups of chronic uremics. In the first control group (31 cases), following a conventional low-protein diet, creatinine clearance declined linearly with time. In the second group (12 cases), following very low nitrogen diet supplemented with essential amino acids and ketoanalogues, creatinine clearance remained practically constant with only one exception in which it continued to decline. In the third group of uremics (13 cases) on repeated dialysis therapy, the deterioration of creatinine clearance was markedly accelerated. The possible explanations and the practical implications of these findings are discussed.

Adolescent↗
PubMed1980

[Chronic renal insufficiency. Low-protein diet supplemented with essential amino acids and ketoanalogues].

Conventional conservative treatment of chronic uremia is aimed at reducing protein intake to a minimum level compatible with nitrogen balance. A great progress in this field is represented by a low protein diet associated with some essential aminoacids and ketoanalogues. A group of 20 patients with chronic renal failure at an advanced stage has been studied and good results have been obtained with a low protein diet (0.2 g/kg/24 h vegetable proteins) associated with essential aminoacids and ketoanalogues.

Amino Acids, Essential↗
PubMed1975

Factors affecting the metabolic production of methylguanidine.

1. Methylguanidine administered orally to normal volunteers was almost completely recovered in the urine, indicating that it is absorbed in the gastrointestinal tract and is not converted into other compounds. In normal persons at least, its urinary output therefore corresponds to its metabolic production rate plus the amount ingested. 2. In normal persons, diets based on foods not containing methylguanidine (e.g. vegetarian, protein-free and milk-egg) caused a fall in the urinary output of methylguanidine as compared with the output of the same subjects on a free diet. Conversely, higher amounts of methylguanidine were excreted on a diet rich in broth and in boiled beef, which contain large amounts of methylguanidine formed from the oxidation of creatinine, caused by boiling. 3. Oral administration of creatinine to normal volunteers induced an immediate and marked increase in urinary excretion of methylguanidine, and the ingestion of [methyl-14-C]creatinine by uraemic patients was followed by the urinary excretion of labelled methylguanidine. These findings indicate that creatinine is partly converted into methylguanidine in both normal and uraemic subjects and accounts for the high metabolic production of methylguanidine in patients with renal failure, in whom the body pool of creatinine is high. 4. Creatinine, incubated at 38 degrees C for 24 h in Krebs bicarbonate solution (pH 7-38) through which was bubbled oxygen with 15% carbon dioxide, was partially oxidized to methylguanidine. This raises the possibility that even in vivo such a conversion may occur "non-enzymatically".

Animals↗