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Biomedical subjects

G Barsotti

Publications and source records attributed to G Barsotti.

11 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↗
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↗
PubMed1975

Uremic intoxication.

The toxic effects of metabolites that are known to accumulate in renal failure are described and the role that they may play in causing uremic symptoms is considered. The opinion of the Authors is that all they are likely to take a lesser or greater part in uremic intoxication. Methylguanidine seems to be very important in this context while for some others (like amines) nothing can be stated for studies on their chronic toxicity are lacking. The hypothesis is also considered of the accumulation of unidentified toxic metabolites with a middle molecular weight. It is stated, as to this problem, that the clinical evidence apparently supporting univocally their existence, is instead also consistent with the hypothesis of toxins (like methylguanidine) having a preferential distribution in the intracellular fluid compartment.

Amines↗
PubMed1975

Removal by dialysis of methylguanidine from body fluids.

The dialysis clearance of methylguanidine (MG) was found to be lower 'in vivo' than 'in vitro' and to decrease during a haemodialysis. Its protein binding, which rises as the plasma pH rises during haemodialysis, accounts for its dialysis behaviour. The low dialysis clearance of MG 'in vivo' explains why the post dialysis percentage decrease in its plasma levels is lower than that of urea (U) and of creatinine (CR). The slow transfer of MG from tissue during dialysis, shown by direct measurements on plasma and muscle tissue of anuric dogs, accounts for its high plasma rebound level after haemodialysis. Rebounds after peritoneal dialysis were lower and the plasma MG levels 12 hr after the termination of the two dialysis procedures were not different. The dialytic behaviour of MG is different from that of U and of CR which have similar molecular weights and the conclusions drawn from the behaviour of the latter two metabolites cannot be applied to MG. On the contrary, the removal of MG from body fluids of uraemic patients by dialysis is equal with peritoneal dialysis and with the various haemodialysis schedules that ensure good clinical results, while leaving plasma U and CR concentrations in a high range.

Animals↗
PubMedDate not supplied

[Dialysis of methylguanidine and hypothesis on the middle molecules].

The formulation of "Methilguanidine (MG) hypothesis" started from previous researches that showed that uramic symptoms in dogs intoxicated by MG were present. Being a low molecular weight molecule, MG as Urea (U) and Creatine (CR), should not be considered an "uraemic toxin" according with the "middle molecules hipothesis". We have studied, during peritoneal and various hemodialysis schedules, MG "in vivo" and "in vitro" clearance, post-dialytic rebound, plasmaaproteins binding, intra and extracellular distribution. "In vitro" MG clearance is intermediate between U and CR, but "in vivo" MG clearance is lower than U and CR: what is explained by MG prevalent intracellular distribution and by the increasing plasm proteins binding during hemodialysis alkalinisation. 12 hours after high efficiency dialysis MG has an higher rebound than U and CR because of the slow and constant MG flow from intracellular fluid to plasma. On the other hand a continuous equilibrium between intra extracellular MG happens during the longer and less efficient peritoneal dialysis: MG plasma level 12 hours after peritoneal dialysis is the same that after high efficiency hemodialysis; on the contrary U and CR plasma levels are higher after peritoneal than after hemodialysis. In spite of the low molecular weight MG dialysis is different than U and CR. Good clinical condition of patients on peritoneal and low-flow-dialysis which represented the basis of the ""MG hypothesis": infact MG removal is the same during peritoneal and hemodialysis.

Animals↗