Search

National and International Societies recommend the Low Protein Diet (LPD) as nutritional therapy for chronic kidney disease not on dialysis, because it reduces the uremic symptoms and toxins generation, preserves the nutritional status, delays the progression to the dialysis and reshapes the dysbiotic microbiota. Finally, LPD is low cost and eco- and planet friendly. As some Authors already described LPD as a traditional drug, with particular indications, contraindications, special populations and so on, we for the first time re-wrote the LPD characteristics according to the “Summary of Product Characteristics” required by the Italian Health Department and Italian Medicines Agency. However, the contents of this paper could not be “literally” applied by clinicians, but must be included in a global assessment of the patient and performed by a trained physician or dietitian with expertise in the management of chronic kidney disease., National and International Societies recommend the Low Protein Diet (LPD) as nutritional therapy for chronic kidney disease not on dialysis, because it reduces the uremic symptoms and toxins generation, preserves the nutritional status, delays the progression to the dialysis and reshapes the dysbiotic microbiota. Finally, LPD is low cost and eco- and planet friendly. As some Authors already described LPD as a traditional drug, with particular indications, contraindications, special populations and so on, we for the first time re-wrote the LPD characteristics according to the “Summary of Product Characteristics” required by the Italian Health Department and Italian Medicines Agency. However, the contents of this paper could not be “literally” applied by clinicians, but must be included in a global assessment of the patient and performed by a trained physician or dietitian with expertise in the management of chronic kidney disease.

National and International Societies recommend the Low Protein Diet (LPD) as nutritional therapy for chronic kidney disease not on dialysis, because it reduces the uremic symptoms and toxins generation, preserves the nutritional status, delays the progression to the dialysis and reshapes the dysbiotic microbiota. Finally, LPD is low cost and eco- and planet friendly. As some Authors already described LPD as a traditional drug, with particular indications, contraindications, special populations and so on, we for the first time re-wrote the LPD characteristics according to the “Summary of Product Characteristics” required by the Italian Health Department and Italian Medicines Agency. However, the contents of this paper could not be “literally” applied by clinicians, but must be included in a global assessment of the patient and performed by a trained physician or dietitian with expertise in the management of chronic kidney disease., National and International Societies recommend the Low Protein Diet (LPD) as nutritional therapy for chronic kidney disease not on dialysis, because it reduces the uremic symptoms and toxins generation, preserves the nutritional status, delays the progression to the dialysis and reshapes the dysbiotic microbiota. Finally, LPD is low cost and eco- and planet friendly. As some Authors already described LPD as a traditional drug, with particular indications, contraindications, special populations and so on, we for the first time re-wrote the LPD characteristics according to the “Summary of Product Characteristics” required by the Italian Health Department and Italian Medicines Agency. However, the contents of this paper could not be “literally” applied by clinicians, but must be included in a global assessment of the patient and performed by a trained physician or dietitian with expertise in the management of chronic kidney disease.

National and International Societies recommend the Low Protein Diet (LPD) as nutritional therapy for chronic kidney disease not on dialysis, because it reduces the uremic symptoms and toxins generation, preserves the nutritional status, delays the progression to the dialysis and reshapes the dysbiotic microbiota. Finally, LPD is low cost and eco- and planet friendly. As some Authors already described LPD as a traditional drug, with particular indications, contraindications, special populations and so on, we for the first time re-wrote the LPD characteristics according to the “Summary of Product Characteristics” required by the Italian Health Department and Italian Medicines Agency. However, the contents of this paper could not be “literally” applied by clinicians, but must be included in a global assessment of the patient and performed by a trained physician or dietitian with expertise in the management of chronic kidney disease., National and International Societies recommend the Low Protein Diet (LPD) as nutritional therapy for chronic kidney disease not on dialysis, because it reduces the uremic symptoms and toxins generation, preserves the nutritional status, delays the progression to the dialysis and reshapes the dysbiotic microbiota. Finally, LPD is low cost and eco- and planet friendly. As some Authors already described LPD as a traditional drug, with particular indications, contraindications, special populations and so on, we for the first time re-wrote the LPD characteristics according to the “Summary of Product Characteristics” required by the Italian Health Department and Italian Medicines Agency. However, the contents of this paper could not be “literally” applied by clinicians, but must be included in a global assessment of the patient and performed by a trained physician or dietitian with expertise in the management of chronic kidney disease.

A key pathogenic role in the development of secondary hyperparathyroidism in renal patients is played by the fibroblast growth factor 23 (FGF23), a 32 kDa protein secreted by osteocytes in response to dietary phosphorus load. FGF23 elicits a phosphaturic response and inhibits calcitriol synthesis. Measurement of FGF23 levels in patients with chronic renal insufficiency can be useful to better define abnormalities of calcium-phosphate metabolism as well as to select those patients in need of dietary interventions targeted to reduce phosphorus intake. Unfortunately, up to now some limits in its application as well as economic factors have prevented the routine use of FGF23 quantification in clinical practice. The aim of our study was to evaluate the circulating levels of FGF23 in patients with chronic kidney disease using the LIAISON® FGF23 (DiaSorin) assay, a new automated chemiluminescence method that measures the intact molecule and has been approved for clinical use. Twenty-three consecutive patients (14 males and 9 females, with mean age 72.3±10.9 years) with stage 3a-5ND CKD were enrolled. The FGF23 assay was also tested in 10 random patients with end-stage renal disease on hemodialysis. Serum levels of FGF23, PTH, 25(OH)VitD, calcium, phosphorus, creatinine and albumin were measured under fasting conditions. Within the CKD group, FGF23 serum levels were higher than normal in 16 cases. Serum FGF23 levels correlated significantly with serum phosphorus (r = 0.600, p, non disponibile

A key pathogenic role in the development of secondary hyperparathyroidism in renal patients is played by the fibroblast growth factor 23 (FGF23), a 32 kDa protein secreted by osteocytes in response to dietary phosphorus load. FGF23 elicits a phosphaturic response and inhibits calcitriol synthesis. Measurement of FGF23 levels in patients with chronic renal insufficiency can be useful to better define abnormalities of calcium-phosphate metabolism as well as to select those patients in need of dietary interventions targeted to reduce phosphorus intake. Unfortunately, up to now some limits in its application as well as economic factors have prevented the routine use of FGF23 quantification in clinical practice. The aim of our study was to evaluate the circulating levels of FGF23 in patients with chronic kidney disease using the LIAISON® FGF23 (DiaSorin) assay, a new automated chemiluminescence method that measures the intact molecule and has been approved for clinical use. Twenty-three consecutive patients (14 males and 9 females, with mean age 72.3±10.9 years) with stage 3a-5ND CKD were enrolled. The FGF23 assay was also tested in 10 random patients with end-stage renal disease on hemodialysis. Serum levels of FGF23, PTH, 25(OH)VitD, calcium, phosphorus, creatinine and albumin were measured under fasting conditions. Within the CKD group, FGF23 serum levels were higher than normal in 16 cases. Serum FGF23 levels correlated significantly with serum phosphorus (r = 0.600, p, non disponibile

A key pathogenic role in the development of secondary hyperparathyroidism in renal patients is played by the fibroblast growth factor 23 (FGF23), a 32 kDa protein secreted by osteocytes in response to dietary phosphorus load. FGF23 elicits a phosphaturic response and inhibits calcitriol synthesis. Measurement of FGF23 levels in patients with chronic renal insufficiency can be useful to better define abnormalities of calcium-phosphate metabolism as well as to select those patients in need of dietary interventions targeted to reduce phosphorus intake. Unfortunately, up to now some limits in its application as well as economic factors have prevented the routine use of FGF23 quantification in clinical practice. The aim of our study was to evaluate the circulating levels of FGF23 in patients with chronic kidney disease using the LIAISON® FGF23 (DiaSorin) assay, a new automated chemiluminescence method that measures the intact molecule and has been approved for clinical use. Twenty-three consecutive patients (14 males and 9 females, with mean age 72.3±10.9 years) with stage 3a-5ND CKD were enrolled. The FGF23 assay was also tested in 10 random patients with end-stage renal disease on hemodialysis. Serum levels of FGF23, PTH, 25(OH)VitD, calcium, phosphorus, creatinine and albumin were measured under fasting conditions. Within the CKD group, FGF23 serum levels were higher than normal in 16 cases. Serum FGF23 levels correlated significantly with serum phosphorus (r = 0.600, p, non disponibile

Whereas the adequate intake of potassium is relatively high in healthy adults, i.e., 4.7 g per day, a dietary potassium restriction of usually less than 3 g per day is recommended in the management of patients with reduced kidney function, especially those who tend to develop hyperkalaemia including patients who are treated with angiotensin pathway modulators. Most potassium-rich foods are considered heart-healthy nutrients with high fibre, high anti-oxidant vitamins and high alkali content such as fresh fruits and vegetables; hence, the main challenge of dietary potassium management is to maintain high fibre intake and a low net fixed-acid load, because constipation and metabolic acidosis are per se major risk factors for hyperkalaemia. To achieve a careful reduction of dietary potassium load without a decrease in alkali or fibre intake, we recommend the implementation of certain pragmatic dietary interventions as follows: Improving knowledge and education about the type of foods with excess potassium (per serving or per unit of weight); identifying foods that are needed for healthy nutrition in renal patients; classification of foods based on their potassium content normalized per unit of dietary fibre; education about the use of cooking procedures (such as boiling) in order to achieve effective potassium reduction before eating; and attention to hidden sources of potassium, in particular additives in preserved foods and low-sodium salt substitutes. The present paper aims to review dietary potassium handling and gives information about practical approaches to limit potassium load in chronic kidney disease patients at risk of hyperkalaemia.

Background and Aim: Obesity, dyslipidemia, hypertension and glucose intolerance are some of the main nutritional and metabolic problems that occur in post-transplant patients. We evaluated the daily dietary intake in renal transplant recipients to assess whether they fulfil the nutrient intake recommendations (according to the Italian recommended dietary allowances, LARN 2014). Subjects and Methods: Renal allograft recipients that were transplanted between 6 months and 5 years before this study were recruited. The daily intake of nutrients, including protein and salt, was estimated with a five-day food diary. Results: In total, 50 patients were studied (31 males and19 females); the mean patients’ age was 48.9±9.9 years, the mean age at transplant was 20.5±15.2 years (median 15.3 y) and the mean eGFR was 56.4±20.2 mL/min/1.73m2, with the eGFR terziles defined as >66.7, between 44.6 and 66.7, and, non disponibile

Background and Aim: Obesity, dyslipidemia, hypertension and glucose intolerance are some of the main nutritional and metabolic problems that occur in post-transplant patients. We evaluated the daily dietary intake in renal transplant recipients to assess whether they fulfil the nutrient intake recommendations (according to the Italian recommended dietary allowances, LARN 2014). Subjects and Methods: Renal allograft recipients that were transplanted between 6 months and 5 years before this study were recruited. The daily intake of nutrients, including protein and salt, was estimated with a five-day food diary. Results: In total, 50 patients were studied (31 males and19 females); the mean patients’ age was 48.9±9.9 years, the mean age at transplant was 20.5±15.2 years (median 15.3 y) and the mean eGFR was 56.4±20.2 mL/min/1.73m2, with the eGFR terziles defined as >66.7, between 44.6 and 66.7, and, non disponibile

Whereas the adequate intake of potassium is relatively high in healthy adults, i.e., 4.7 g per day, a dietary potassium restriction of usually less than 3 g per day is recommended in the management of patients with reduced kidney function, especially those who tend to develop hyperkalaemia including patients who are treated with angiotensin pathway modulators. Most potassium-rich foods are considered heart-healthy nutrients with high fibre, high anti-oxidant vitamins and high alkali content such as fresh fruits and vegetables; hence, the main challenge of dietary potassium management is to maintain high fibre intake and a low net fixed-acid load, because constipation and metabolic acidosis are per se major risk factors for hyperkalaemia. To achieve a careful reduction of dietary potassium load without a decrease in alkali or fibre intake, we recommend the implementation of certain pragmatic dietary interventions as follows: Improving knowledge and education about the type of foods with excess potassium (per serving or per unit of weight); identifying foods that are needed for healthy nutrition in renal patients; classification of foods based on their potassium content normalized per unit of dietary fibre; education about the use of cooking procedures (such as boiling) in order to achieve effective potassium reduction before eating; and attention to hidden sources of potassium, in particular additives in preserved foods and low-sodium salt substitutes. The present paper aims to review dietary potassium handling and gives information about practical approaches to limit potassium load in chronic kidney disease patients at risk of hyperkalaemia.

The Italian nephrology has a long tradition and experience in the field of dietetic-nutritional therapy (DNT), which is an important component in the conservative management of the patient suffering from a chronic kidney disease, which precedes and integrates the pharmacological therapies. The objectives of DNT include the maintenance of an optimal nutritional status, the prevention and/or correction of signs, symptoms and complications of chronic renal failure and, possibly, the delay in starting of dialysis. The DNT includes modulation of protein intake, adequacy of caloric intake, control of sodium and potassium intake, and reduction of phosphorus intake. For all dietary-nutritional therapies, and in particular those aimed at the patient with chronic renal failure, the problem of patient adherence to the dietetic-nutritional scheme is a key element for the success and safety of the DNT and it can be favored by an interdisciplinary and multi-professional approach of information, education, dietary prescription and follow-up. This consensus document, which defines twenty essential points of the nutritional approach to patients with advanced chronic renal failure, has been written, discussed and shared by the Italian nephrologists together with representatives of dietitians (ANDID) and patients (ANED).

Background and Aim: Obesity, dyslipidemia, hypertension and glucose intolerance are some of the main nutritional and metabolic problems that occur in post-transplant patients. We evaluated the daily dietary intake in renal transplant recipients to assess whether they fulfil the nutrient intake recommendations (according to the Italian recommended dietary allowances, LARN 2014). Subjects and Methods: Renal allograft recipients that were transplanted between 6 months and 5 years before this study were recruited. The daily intake of nutrients, including protein and salt, was estimated with a five-day food diary. Results: In total, 50 patients were studied (31 males and19 females); the mean patients’ age was 48.9±9.9 years, the mean age at transplant was 20.5±15.2 years (median 15.3 y) and the mean eGFR was 56.4±20.2 mL/min/1.73m2, with the eGFR terziles defined as >66.7, between 44.6 and 66.7, and, non disponibile

Adamasco Cupisti, Valentina Vigo, Maria Enrica Baronti, Claudia D'Alessandro, Lorenzo Ghiadoni, Maria Francesca Egidi Nephrology, Transplant and Dialysis Division, AOUP, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy Abstract: This study investigated the factors associated with hypovitaminosis D, in a cohort of 405 prevalent patients with chronic kidney disease (CKD) stages 2–4, living in Italy and followed-up in tertiary care. The effect of cholecalciferol 10,000 IU once-a-week for 12 months was evaluated in a subgroup of 100 consecutive patients with hypovitaminosis D. Vitamin D deficiency was observed in 269 patients (66.4%) whereas vitamin D insufficiency was found in 67 patients (16.5%). In diabetic patients, 25-hydroxyvitamin D deficiency was detected in 80% of cases. In patients older than 65 years, the prevalence of hypovitaminosis D was 89%. In the univariate analysis, 25-hydroxyvitamin D was negatively related to age, parathyroid hormone (PTH), proteinuria, and Charlson index, while a positive relationship has emerged with hemoglobin level. On multiple regression analysis, only age and PTH levels were independently associated with 25-hydroxyvitamin D levels. No relationship emerged between vitamin D deficiency and renal function. Serum levels of 25-hydroxyvitamin D or prevalence of hypovitaminosis D did not differ between patients on a free-choice diet and on a renal diet, including low-protein, low-phosphorus regimens. Twelve-month oral cholecalciferol administration increased 25-hydroxyvitamin D and reduced PTH serum levels. In summary, hypovitaminosis D is very prevalent in CKD patients (83%) in Italy, and it is similar to other locations. PTH serum levels and age, but not renal function, are the major correlates of hypovitaminosis D. Implementation of renal diets is not associated with higher risk of vitamin D depletion. Oral cholecalciferol administration increased 25-hydroxyvitamin D and mildly red

Adamasco Cupisti, Valentina Vigo, Maria Enrica Baronti, Claudia D'Alessandro, Lorenzo Ghiadoni, Maria Francesca Egidi Nephrology, Transplant and Dialysis Division, AOUP, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy Abstract: This study investigated the factors associated with hypovitaminosis D, in a cohort of 405 prevalent patients with chronic kidney disease (CKD) stages 2–4, living in Italy and followed-up in tertiary care. The effect of cholecalciferol 10,000 IU once-a-week for 12 months was evaluated in a subgroup of 100 consecutive patients with hypovitaminosis D. Vitamin D deficiency was observed in 269 patients (66.4%) whereas vitamin D insufficiency was found in 67 patients (16.5%). In diabetic patients, 25-hydroxyvitamin D deficiency was detected in 80% of cases. In patients older than 65 years, the prevalence of hypovitaminosis D was 89%. In the univariate analysis, 25-hydroxyvitamin D was negatively related to age, parathyroid hormone (PTH), proteinuria, and Charlson index, while a positive relationship has emerged with hemoglobin level. On multiple regression analysis, only age and PTH levels were independently associated with 25-hydroxyvitamin D levels. No relationship emerged between vitamin D deficiency and renal function. Serum levels of 25-hydroxyvitamin D or prevalence of hypovitaminosis D did not differ between patients on a free-choice diet and on a renal diet, including low-protein, low-phosphorus regimens. Twelve-month oral cholecalciferol administration increased 25-hydroxyvitamin D and reduced PTH serum levels. In summary, hypovitaminosis D is very prevalent in CKD patients (83%) in Italy, and it is similar to other locations. PTH serum levels and age, but not renal function, are the major correlates of hypovitaminosis D. Implementation of renal diets is not associated with higher risk of vitamin D depletion. Oral cholecalciferol administration increased 25-hydroxyvitamin D and mildly red

The modulator of the sea urchin alpha-H2A histone gene promoter is the only enhancer identified in the alpha-histone gene cluster. Binding of a single factor, denoted MBF-1, has previously detected in nuclear extracts from morula and gastrula embryos. Here, we describe the cloning of MBF-1 by screening a cDNA expression library with a tandem array of modulator binding sites. MBF-1 presents no similarity with other DNA binding proteins and contains nine Krüppel like Zn fingers. In vitro translated proteins and a factor from nuclear extracts interact with the modulator with identical specificity. In addition, MBF-1 expressed in human cells transactivates a reporter gene driven by an array of modulator sites. The DNA binding domain consists of the Zn fingers plus an adjacent basic region, while sequences in the N-terminal region mediates the transactivation function. MBF-1 is expressed in the unfertilized egg and in early and late developmental stages thus confirming that it is not a stage specific enhancer binding factor and that silencing of the alpha-H2A gene after hatching is not due to the lack of the transactivator.