Abstract:Serum iPTH levels decreased markedly in 16 severe chronic uremic patients who changed from a standard low-protein diet to a very low-nitrogen and very low-phosphorus diet supplemented with essential amino acids and keto-analogues and with calcium. The fall of serum iPTH levels occurred simultaneously with a fall of serum phosphate and an increase of serum calcium.
“…These results confirm our previous observations of a similar effect exerted by dietary treatment on circulating NH 2 - and C-terminal PTH fragments [4]. More recently, Lafage et al [6] and Combe and Aparicio [7] demonstrated the reversal of secondary hyperparathyroidism and some favorable effects on bone metabolism exerted by a similar dietary regimen associated with native vitamin D administration.…”
Section: Discussionsupporting
confidence: 90%
“…Therefore, correction of hyperphosphatemia and hypocalcemia by lowering dietary phosphorus intake and by the administration of calcium-containing phosphate binders is the first target of therapeutic intervention [4], whereas the use of vitamin D derivatives is questionable, in predialysis patients at least [5]. …”
The main purpose of our study was to verify the effect of a very-low-protein, low-phosphorus diet, supplemented with essential amino acids and keto analogues and with calcium carbonate, on circulating levels of intact parathyroid hormone (i-PTH) in severe chronic renal failure patients with secondary hyperparathyroidism, not treated with any vitamin D preparation. To this aim, we shifted 21 chronic uremics (12 males, 9 females; age 56 ± 13 years) with serum creatinine >6.5 mg/dl and i-PTH >150 pg/ml, from a standard low-protein diet (0.6 g/kg/day approximately) to a very-low-protein (0.3 g/kg/day), very-low-phosphorus (5 mg/kg/day) diet supplemented with a mixture of essential amino acids and calcium keto analogues (Ketodiet), calcium carbonate (2–4 g/day), iron, and vitamin B12 preparations. The energy supply of both diets was 30–35 kcal/kg/day. Exclusion criteria were a poor compliance with dietary or supplement prescriptions or signs of autonomic hyperparathyroidism. After 4 ± 2 months of Ketodiet, the i-PTH serum levels decreased by 49% as a mean (from 441 ± 233 to 225 ± 161 pg/ml, p < 0.001); serum phosphorus and alkaline phosphatase decreased, whereas serum calcium increased. The great reduction of serum and urinary urea demonstrated a good compliance with Ketodiet, and no sign of protein malnutrition was observed. These findings confirm that even in severe chronic uremic patients dietary phosphorus restriction and calcium carbonate supplementation lower i-PTH serum levels. This is one of the goals of the dietary treatment that can be safely achieved, provided good compliance both with the dietary prescriptions and with adequate energy and supplement intakes.
“…These results confirm our previous observations of a similar effect exerted by dietary treatment on circulating NH 2 - and C-terminal PTH fragments [4]. More recently, Lafage et al [6] and Combe and Aparicio [7] demonstrated the reversal of secondary hyperparathyroidism and some favorable effects on bone metabolism exerted by a similar dietary regimen associated with native vitamin D administration.…”
Section: Discussionsupporting
confidence: 90%
“…Therefore, correction of hyperphosphatemia and hypocalcemia by lowering dietary phosphorus intake and by the administration of calcium-containing phosphate binders is the first target of therapeutic intervention [4], whereas the use of vitamin D derivatives is questionable, in predialysis patients at least [5]. …”
The main purpose of our study was to verify the effect of a very-low-protein, low-phosphorus diet, supplemented with essential amino acids and keto analogues and with calcium carbonate, on circulating levels of intact parathyroid hormone (i-PTH) in severe chronic renal failure patients with secondary hyperparathyroidism, not treated with any vitamin D preparation. To this aim, we shifted 21 chronic uremics (12 males, 9 females; age 56 ± 13 years) with serum creatinine >6.5 mg/dl and i-PTH >150 pg/ml, from a standard low-protein diet (0.6 g/kg/day approximately) to a very-low-protein (0.3 g/kg/day), very-low-phosphorus (5 mg/kg/day) diet supplemented with a mixture of essential amino acids and calcium keto analogues (Ketodiet), calcium carbonate (2–4 g/day), iron, and vitamin B12 preparations. The energy supply of both diets was 30–35 kcal/kg/day. Exclusion criteria were a poor compliance with dietary or supplement prescriptions or signs of autonomic hyperparathyroidism. After 4 ± 2 months of Ketodiet, the i-PTH serum levels decreased by 49% as a mean (from 441 ± 233 to 225 ± 161 pg/ml, p < 0.001); serum phosphorus and alkaline phosphatase decreased, whereas serum calcium increased. The great reduction of serum and urinary urea demonstrated a good compliance with Ketodiet, and no sign of protein malnutrition was observed. These findings confirm that even in severe chronic uremic patients dietary phosphorus restriction and calcium carbonate supplementation lower i-PTH serum levels. This is one of the goals of the dietary treatment that can be safely achieved, provided good compliance both with the dietary prescriptions and with adequate energy and supplement intakes.
“…LPD was low in cysteine and methionine, and therefore had a low acid content. Barsotti et al [30,31] have shown that correcting metabolic acidosis induces reduction in plasma phosphate level without any change in the body pool of phosphate. This probably results from the translocation of phosphate from an extracellular to an intracellular site.…”
Aim: To evaluate the effects of short-term restriction of dietary protein intake (DPI) supplemented with keto acids on hyperphosphatemia in maintenance hemodialysis (MHD) patients. Methods: Forty MHD patients with uncontrolled hyperphosphatemia were randomized to either low DPI with keto acid-supplemented (sLP) or normal DPI (NP) group for 8 weeks. After 8 weeks, the sLP group was shifted to NP for another 8 weeks. Low-protein diet (LPD) was individualized with total caloric intake 30–35 kcal/kg/day, protein intake of 0.8 g/kg/day and phosphate intake of 500 mg/day. Keto acids were supplied in a dosage of 12 pills per day. Calcium phosphorous metabolism index and nutritional index (serum albumin, total protein, somatometric measurements, 3-day diaries and Mini-Nutritional Assessment score) were recorded. C-reactive protein, CO2 combining power and Kt/V were measured to evaluate the inflammation, metabolic acidosis and dialysis adequacy, respectively. Results: Serum phosphorus level and calcium-phosphate product were significantly decreased at the end of the first 8 weeks in the sLP group compared to the basal value and the NP group (p < 0.001). No difference was observed in C-reactive protein, Kt/V and nutritional index, while CO2 combining power was significantly higher at week 8 in the sLP group (p < 0.001). Conclusion: Short-term restriction of DPI supplemented with keto acids could decrease hyperphosphatemia and calcium-phosphate product, while keeping stable nutritional status among MHD patients.
“…These patients had been undergoing conservative therapy from ten to 22 months when the initial study was carried out. They were following a nitrogen-restricted diet containing high quality, low phosphorus proteins or keto-analogs of essential amino acids (Giovannetti and Maggiore, 1964;Barsotti et al, 1982). During this treatment, their serum creatinine ranged from 4 to 8 mg/lOO ml.…”
Twenty patients with sexual inadequacies secondary to different degrees of chronic renal failure were investigated. The patients were divided into two groups: group A—ten patients treated with a conservative diet therapy; group B—ten patients on hemodialysis. All the patients under investigation were administered 2000 IU of hCG every other day for 120 days after a 30‐day period without treatment. Andrologic, biometric, hematologic, and sexual data were evaluated before and after hormone treatment. Sexual parameters were collected through self‐evaluation by the patients and their partners.
Our results agree with Van Kammen et al (1975) and show an improvement of the andrologic and biometric data in patients from group A. Furthermore, eight patients form group A and three patients from group B reported a remarkable improvement in their sexual responses.
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