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Biomedical subjects

G Barsotti

Publications and source records attributed to G Barsotti.

At least 19 recordsLinked to original sources
PubMed1992

Low urine citrate excretion as main risk factor for recurrent calcium oxalate nephrolithiasis in males.

To better define the relative role of metabolic factors in the recurrence of stone formation, we studied the 24-hour urinary excretion of calcium (uCa), citrate (uCit), oxalic acid (uOx) and uric acid (uUa) in 73 male patients with primary calcium oxalate urolithiasis. According to the episodes of stone formation per year, we identified 51 recurrent stone formers (RSF) and 22 single stone formers (SSF). 20 normal adult males constituted the control group (C). uCa and uOx were higher in RSF than in C, but quite similar in SSF and RSF. The only difference between RSF and SSF was uCit, significantly lower (2.06 +/- 1.04 mmol/24 h) in RSF than in SSF (3.22 +/- 1.18 mmol/24 h, p less than 0.001) and in C (3.42 +/- 1.33 mmol/24 h, p less than 0.001). Hypocitraturia (uCit less than 1.5 mmol/24 h) was found in 16 of 51 RSF (31.4%) and in 1 of 22 SSF (4.5%). These data confirm that high levels of uCa and uOx represent a risk factor for lithogenesis, but also strongly indicate the low uCit excretion as the most important urinary abnormality accounting for the recurrence of calcium oxalate stones.

Adult↗
PubMed1991

A special, supplemented 'vegan' diet for nephrotic patients.

High dietary protein intake, in the past recommended for nephrotic syndrome, does not improve hypoproteinemia and may accelerate progressive renal damage. In contrast, low-protein diets reduce proteinuria and preserve renal function in experimental renal models of nephrotic syndrome. In this study, 20 steroid-resistant, nephrotic patients were treated with a pure vegetarian, low-protein diet, supplemented with essential amino acids and ketoanalogues (supplemented vegan diet, SVD) for 4.6 +/- 3.1 months. Before the study, these patients followed an unrestricted protein, low-sodium diet (LSD). Proteinuria, daily urea nitrogen excretion and creatinine clearance decreased significantly on SVD. A similar lowering effect of SVD was observed on serum total cholesterol. Seven of the 20 patients changed from LSD to SVD and vice-versa on 3 occasions, and in all cases, we found an increase of proteinuria during the LSD period. Serum albumin, HDL cholesterol, triglycerides and anthropometric measurements did not change on SVD. Our data suggest that SVD exerts a favorable effect on proteinuria and hypercholesterolemia in nephrotic patients, without inducing clinical or laboratory signs of malnutrition.

Adult↗
PubMed1991

In defense of creatinine clearance.

The ratios creatinine clearance (Crcl)/inulin clearance (INcl) obtained in 523 measurements and reported in 14 papers have been analyzed and the values of CRcl corresponding to those of INcl have been evaluated. The day-to-day coefficient of variation of CRcl has also been measured in 123 persons, including patients with stable chronic renal failure and patients with normal renal function. The data obtained indicate that CRcl is not less sensitive than INcl, and that its changes are not blunted, if compared with similar changes of INcl. The day-to-day coefficient of variation has been found not to be greater than that of INcl. In conclusion, CRcl is not a misleading method to obtain approximate information on renal function, if it is correctly executed and interpreted.

Creatinine↗
PubMed1990

Vegan supplemented diet in nephrotic syndrome.

Thirteen patients (7 males, 6 females, aged 17-68 years) affected by primary, steroid-resistant, nephrotic syndrome and normal renal function were treated with a vegan, low-protein (0.7 g/kg per day) diet supplemented with essential amino acids and Ketoanalogues (VSD) for 3.9 +/- 2.9 months. These patients were studied at the beginning (following an unrestricted protein diet (UPD) supplying about 1 g/kg per day of mixed proteins) and at the end of VSD period. Urinary protein excretion decreased from 8.7 +/- 2.6 to 5.6 +/- 2.4 g/day (P less than 0.01), serum total cholesterol from 334.6 +/- 97.1 to 275.6 +/- 49.4 mg/dl (P less than 0.05). Serum albumin, HDL-cholesterol, triglycerides, and anthropometric measurements (triceps skinfold thickness and middle arm muscle circumference) did not change. Urinary urea nitrogen decreased from 7.5 +/- 1.8 to 3.8 +/- 1.2 g/day (P less than 0.005), according to dietary prescriptions. Creatinine clearance changed from 104.4 +/- 28.7 to 89.3 +/- 16.7 ml/min (n.s.) and no correlation was found with the changes in urinary protein excretion. This data suggest that VSD reduces proteinuria and exerts favourable effects on hypercholesterolaemia. Protein malnutrition was absent in these patients, probably because of the essential amino acids and ketoanalogues supplementation.

Adolescent↗
PubMed1989

Molecular markers of hemostasis activation in nephrotic syndrome.

Fibrinopeptide A (FPA), a sensitive index of in vivo thrombin activity, beta-thromboglobulin (beta TG) and platelet factor 4 (PF4), specific markers of platelet intravascular activation, have been measured in plasma by radioimmunoassays in 23 patients with nephrotic syndrome and in 32 normal subjects. FPA concentration was 2.40 +/- 1.42 ng/ml (mean +/- SD) in nephrotic patients and 1.16 +/- 0.58 ng/ml in normal controls (p less than 0.001); beta TG concentration was 57.9 +/- 33.2 ng/ml in nephrotic patients and 25.7 +/- 7.4 ng/ml in controls (p less than 0.001); PF4 level was not different from controls. These data indicate in vivo blood hypercoagulability and platelet hyperfunction in nephrotic syndrome. Moreover, we have documented a slow in vitro FPA generation pattern (delta FPA): 0.97 +/- 0.51 ng/ml/10 min; this suggests that thrombin activity is predominantly local.

Adolescent↗
PubMed1989

Effects of a low-phosphorus, low-nitrogen diet supplemented with essential amino acids and ketoanalogues on serum beta-endorphin in chronic renal failure.

The effects of a vegetarian low-protein, low-phosphorus diet supplemented with essential amino acids and ketoanalogues, on the serum beta-endorphin, growth hormone, parathyroid hormone, thyroid hormones (T3 and T4), pituitary TSH and total cortisol were studied in 12 male chronic uremics. beta-Endorphin decreased, as well as growth hormone. Parathyroid hormone and T3 improved significantly, reaching almost normal values. It is hypothesized that the correction of the beta-endorphin excess may account in part for the improvement of some endocrinological and metabolic effects exerted by this dietary treatment. The possible pathophysiological mechanisms which could explain the antiendorphinic action of this treatment in uremic patients are discussed, as well as the possible beneficial endocrine and metabolic effects exerted by the fall in circulating beta-endorphin.

Adolescent↗
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↗
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↗