Cardiovascular implantable electronic devices and native arteriovenous fistula in hemodialysis patients: novel perspectives.

The benefits from cardiovascular implantable electronic devices (CIED) implantation in hemodialysis (HD) patients are still far to be thoroughly defined, especially on primary prevention. In addition, CIED placement is not a risk-free procedure, because it could be followed by a not negligible burden of complications that could compromise the health and the vascular access of HD patients. In fact, the arteriovenous fistula (AVF) dysfunction following CIED implantation is usually due to a hemodynamically significant alteration of blood flow. This condition could lead to a potential decrease of dialysis efficacy and a raised risk of thrombosis of both the central vein and the efferent vein of the AVF.The pathological pathway that leads to AVF dysfunction after CIED implantation may involve the irritating actions of the CIED and their leads to the vascular wall in HD patients that are more prone to show previous vascular diseases.The aim of this review is to focus the physiopathology of the CIED-induced AVF dysfunction, the current treatment strategies and the novel perspectives that could be taken into consideration and offered to the HD population to preserve both their AVF and their quality of life.

[Clinical management of anemia in patients with CKD].

Anemia is a frequent complication in chronic kidney disease (CKD), and it is often accompanied by various clinical symptoms. The primary cause of anemia in CKD patients is the reduction in the erythropoietin production, which results in a decrease of signaling molecule that stimulates red blood cell production. Other possible causes of anemia in CKD include iron deficiency, inflammation, and the accumulation of uremic toxin. This chapter focuses the discussion on the strategy of the management of anemia in patients with CKD. Erythropoiesis-stimulating agents (ESAs) and adjuvant iron therapy represent the primary treatment for anemia in chronic kidney disease. The introduction of ESAs into clinical practice was a success goal, mediating an increase in hemoglobin concentrations without the risk for recurrent blood transfusions and improving quality of life substantially.

Progression of cardiac valve calcification and decline of renal function in CKD patients.

BACKGROUND: No study has evaluated the efficacy of non-calcium-containing phosphate binders in slowing progression of cardiac valve calcification or deterioration of kidney function in patients with chronic kidney disease not on dialysis. This study addressed these issues. METHODS: Outpatients (n = 170) with stage 3-4 chronic kidney disease and either mitral or aortic valve calcification were evaluated in this single-center, single-arm, prospective observational study. Patients received sevelamer hydrochloride (1,600 mg/day) for 1 year. Cardiac valve calcification progression was assessed by echocardiography, and decline of renal function by estimated glomerular filtration rate. Parathyroid hormone, FGF-23 and C-reactive protein (CRP) serum concentration and urinary phosphorus excretion were assayed. RESULTS: At the end of treatment with sevelamer (12th month), mitral valve calcification had decreased by 79.3% from baseline. At baseline, 69 patients had grade 1, 97 patients grade 2 and 4 patients grade 3 calcification scores; at the end of the study, 60 patients showed grade 1, and no mitral valve calcification was registered in the remaining patients. An aortic valve score of 1 was found in 32%, score of 2 in 58%, score of 3 in 9% and score of 4 in 1% of patients at baseline; at the end of the study, a score of 1 was found in 95% and a score of 2 in 5% of patients. Significant slowing down of renal function decline (p<0.001), reduction of FGF-23 and CRP concentration (p<0.0001) and phosphorus excretion (p<0.0001) were observed. CONCLUSIONS: One-year treatment with a non-calcium-containing phosphate binder may hamper the progression of cardiac valve calcification and slow the decline of renal function, as well as reduce serum concentration of FGF-23 and CRP and urinary phosphorus excretion.