BackgroundNutritional treatment has always represented a major feature of CKD management. Over the decades, the use of nutritional treatment in CKD patients has been marked by several goals. The first of these include the attainment of metabolic and fluid control together with the prevention and correction of signs, symptoms and complications of advanced CKD. The aim of this first stage is the prevention of malnutrition and a delay in the commencement of dialysis. Subsequently, nutritional manipulations have also been applied in association with other therapeutic interventions in an attempt to control several cardiovascular risk factors associated with CKD and to improve the patient's overall outcome. Over time and in reference to multiple aims, the modalities of nutritional treatment have been focused not only on protein intake but also on other nutrients.DiscussionThis paper describes the pathophysiological basis and rationale of nutritional treatment in CKD and also provides a report on extensive experience in the field of renal diets in Italy, with special attention given to approaches in clinical practice and management.SummaryItalian nephrologists have a longstanding tradition in implementing low protein diets in the treatment of CKD patients, with the principle objective of alleviating uremic symptoms, improving nutritional status and also a possibility of slowing down the progression of CKD or delaying the start of dialysis. A renewed interest in this field is based on the aim of implementing a wider nutritional therapy other than only reducing the protein intake, paying careful attention to factors such as energy intake, the quality of proteins and phosphate and sodium intakes, making today’s low-protein diet program much more ambitious than previous. The motivation was the reduction in progression of renal insufficiency through reduction of proteinuria, a better control of blood pressure values and also through correction of metabolic acidosis. One major goal of the flexible and innovative Italian approach to the low-protein diet in CKD patients is the improvement of patient adherence, a crucial factor in the successful implementation of a low-protein diet program.

Abstract. Balloon angioplasty (PTA) is an established treatment modality for stenosis in dysfunctional arteriovenous fistulae (AVF), although most studies showing efficacy have been retrospective, uncontrolled, and nonrandomized. In addition, it is unknown whether correction of stenosis not associated with significant hemodynamic, functional, and clinical abnormality may improve survival in AVF. This study was a prospective controlled open trial to evaluate whether prophylactic PTA of stenosis not associated with access dysfunction improves survival in native, virgin, radiocephalic forearm AVF. Sixty-two stenotic, functioning AVF, i.e., able to provide adequate dialysis, were enrolled in the study: 30 were allocated to control and 32 to PTA. End points of the study were either AVF thrombosis or surgical revision due to reduction in delivered dialysis dose. Kaplan-Meier analysis showed that PTA improved AVF functional failure-free survival rates (P ϭ 0.012) with a fourfold increase in median survival and a 2.87-fold decrease in risk of failure. Cox proportional hazard model identified PTA as the only variable associated with outcome (P ϭ 0.012). PTA induced an increase in access blood flow rate (Qa) by 323 (236 to 445) ml/min (P Ͻ 0.001), suggesting that improved AVF survival is the result of increased Qa. PTA was also associated with a significant decrease in access-related morbidity by approximately halving the risk of hospitalization, central venous catheterization, and thrombectomy (P Ͻ 0.05). This study shows that prophylactic PTA of stenosis in functioning forearm AVF improves access survival and decreases access-related morbidity, supporting the usefulness of preventive correction of stenosis before the development of access dysfunction. It also strongly supports surveillance program for early detection of stenosis.

Three groups of patients with chronic renal failure were studied. Group 1 comprised 25 patients with a mean serum creatinine of 2.18 mg/dl and a mean arterial pressure of 117 mm Hg. Group 2 had 20 patients with a mean serum creatinine of 4.24 mg/dl and a mean arterial pressure of 119 mm Hg. All these patients were kept for 18 to 76 months on a diet containing about 40 kcal/kg, 0.6 g/kg of protein, 700 mg of phosphorus, and 1,000 to 1,500 mg of calcium (orally supplemented). Group 3 comprised 30 patients with a mean serum creatinine of 2.28 mg/dl and a mean arterial pressure of 116 mm Hg. They had followed no specific dietary regimen for 3 to 72 months, and their dietary calorie, protein, phosphorus, and calcium intakes averaged 35 kcal/kg, 70 g, 900 mg, and 800 mg, respectively. The plots of reciprocal creatinine against time gave slopes of -0.0008 and -0.0010 in patients in groups 1 and 2, and a slope of -0.020 in group 3 patients. The slopes of both groups 1 and 2 were statistically different (analysis of variance and "F" test, P less than 0.01) from that of group 3. No evidence of progressive protein and phosphorus depletion was observed in groups 1 and 2 patients. We conclude that a moderate dietary restriction of protein and phosphorus is an acceptable and effective regimen for delaying progression of functional deterioration in early renal failure.

This study shows that anaemia prevalence is unexpectedly high in the setting of tertiary nephrology care. This was due to a persistent clinical inertia in the anaemia management, remarkable for iron supplementation and less critical, but still significant, for ESA treatment.