Low protein diet and progression of chronic renal failure.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S Giovannetti.
Explore the source record for details and available documents.
A low-protein, low-phosphorus diet supplemented with essential amino acids and keto analogues was given to 12 rats, starting from the 90th day after subtotal nephrectomy. The purpose was to assess its effect on the residual renal function and on the nutritional status in rats with already established severe renal failure. Ten control rats in the same conditions, following a standard diet supplying normal amounts of protein and phosphorus were also studied. The supplemented diet exerted a well-evident protection of residual renal function and structure: lower rate of decline of creatinine clearance, lower mortality, significant decrease of proteinuria and almost total absence of histological signs of activity. The nutritional status was also well protected by the dietary therapy: increase of body weight, normal values of total serum protein, and low-constant values of urea appearance. In the control rats body weight decreased, total serum protein was lower than normal and the values of urea appearance were increasing simultaneously with a decreasing food intake and body weight.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
This study reports the effects of a low-protein, low-phosphorus, supplemented diet in 8 type 1 diabetics with renal failure. The rate of decline of creatinine clearance, the changes of the urinary protein loss, of total serum protein, of the daily insulin requirement, of the nutritional status and of some hormonal derangements were examined. The rate of decline of creatinine clearance decreased from 1.38 +/- 0.27 ml/min/month during a previous 15.9-month period of unrestricted protein diet, to 0.03 +/- 0.37 ml/min/month during the 17.4 months on supplemented diet. Urinary protein loss significantly decreased, and total serum protein increased. The daily insulin requirement decreased and no deterioration of the nutritional status occurred. Secondary hyperparathyroidism was partially reversed and the mild hypothyroidism corrected. A restricted protein and phosphorus diet supplemented with essential amino acids and ketoanalogs seems to exert several beneficial and no unwanted side effects in type 1 diabetics with renal failure.
The results are described of a combined nutritional (supplemented diet) and dialytic (once a week hemodialysis) therapy, employed in 17 selected chronic uremics for a mean period of 18.2 months/patient. The clinical findings, blood chemical abnormalities and changes of renal function were examined and compared with those of patients on the standard thrice-a-week dialysis schedule and free diet. The clinical findings were not significantly different in the two groups. The residual renal function of patients on combined therapy declined faster than in patients on conservative treatment, but at a slower rate than in those on thrice-a-week dialysis. The time averages of serum urea, methylguanidine and phosphate concentrations and their postdialytic rebounds were lower in the patients on combined therapy than in those on thrice-a-week dialysis, whereas the time averages of the serum creatinine concentration were higher, and those of serum bicarbonate and serum oxalate were not significantly different in the two groups. It is concluded that this combined therapy is a valid alternative to the conventional thrice-a-week hemodialysis and free diet for selected patients and for periods of time whose duration is conditioned by the rate of decline of the residual renal function.
The compliance with the low-protein, supplemented diet is facilitated or hindered by psychological, social and toxic (severe uremia) factors; however, the most important factor which induces good compliance in patients is the fear of dialysis. The early effect of poor compliance is the appearance of intoxication related to renal failure and the consequent appearance of the uremic syndrome. The assessment of compliance with the low-protein intake is done quite easily by measuring urea appearance; however, regular clinical and laboratory controls are mandatory: anthropometric measurements, evaluation of the serum concentrations of proteins (especially those having a rapid turnover), and the evaluation of thyroid function--which is depressed in a state of malnutrition and improves following nutritional therapy--are adequate for detecting a state of malnutrition following poor compliance.
In this paper we studied the effects of a low-protein, low-phosphorus supplemented diet in 8 type I diabetics with 'overt' diabetic nephropathy and mild or severe renal insufficiency. We examined the following parameters: the rate of decline of creatinine clearance, the urinary protein loss, the total serum protein, the daily insulin requirement, the serum fasting glucose, the pattern of serum lipids (serum total cholesterol, HDL cholesterol and serum triglycerides), the mean blood pressure and body weight. The rate of decline of creatinine clearance decreased monthly from 1.48 +/- 0.20 ml/min during a previous 15.6-month period of unrestricted protein diet (UPD), to 0.13 +/- 0.3 ml/min during the 11.4 months on the supplemented diet (SD). The mean blood pressure did not differ during UPD (130.9 +/- 7.0 mmHg) and during SD (128.1 +/- 1.6 mmHg). Urinary protein loss significantly decreased on SD, and total serum protein increased. The daily insulin requirement and the serum fasting glucose levels significantly decreased on SD. Serum cholesterol was lower during SD than during UPD, while serum HDL cholesterol and serum triglycerides were not significantly modified. In some patients the body weight decreased on SD as a consequence of the disappearance of edema. In conclusion, on the basis of these preliminary observations, the SD slows the progression of renal failure and seems to exert several beneficial and no unwanted side-effects in renal failure of type I diabetics.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
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.
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.