Fibroblast growth factor 21 (FGF21), a 181 amino acid circulating protein, is a member of the FGF superfamily, with relevant metabolic actions. It acts through the interaction with specific FGF receptors and a cofactor called β-Klotho, whose expression is predominantly detected in metabolically active organs. FGF21 stimulates glucose uptake in adipocytes via the induction of glucose transporter-1. This action is additive and independent of insulin. β-Cell function and survival are preserved, and glucagon secretion is reduced by this protein, thus decreasing hepatic glucose production and improving insulin sensitivity. Lipid profile has been shown to be improved by FGF21 in several animal models. FGF21 increases energy expenditure in rodents and induces weight loss in diabetic nonhuman primates. It also exerts favorable effects on hepatic steatosis and reduces tissue lipid content in rodents. Adaptive metabolic responses to fasting, including stimulation of ketogenesis and fatty acid oxidation, seem to be partially mediated by FGF21. In humans, serum FGF21 concentrations have been found elevated in insulin-resistant states, such as impaired glucose tolerance and type 2 diabetes. FGF21 levels are correlated with hepatic insulin resistance index, fasting blood glucose, HbA1c, and blood glucose after an oral glucose tolerance test. A relationship between FGF21 levels and long-term diabetic complications, such as nephropathy and carotid atheromatosis, has been reported. FGF21 levels decreased in diabetic patients after starting therapy with insulin or oral agents. Increased FGF21 serum levels have also been found to be associated with obesity. In children, it is correlated with BMI and leptin levels, whereas in adults, FGF21 levels are mainly related to several components of the metabolic syndrome. Serum FGF21 levels have been found to be elevated in patients with ischemic heart disease. In patients with renal disease, FGF21 levels exhibited a progressive increase as renal function deteriorates. Circulating FGF21 levels seem to be related to insulin resistance and inflammation in dialysis patients. In summary, FGF21 is a recently identified hormone with antihyperglycemic, antihyperlipidemic, and thermogenic properties. Direct or indirect potentiation of its effects might be a potential therapeutic target in insulin-resistant states.

Our study shows that daily peritoneal PrC on initiating PD is significantly and independently related to the presence of PAD. Peritoneal PrC appears to be a possible new marker of systemic endothelial dysfunction.

The treatment of cirrhotic patients with ascites and end-stage renal disease is complex, due mainly to decreased effective arterial volume and hemodynamic instability. Peritoneal dialysis as a continuous therapy represents an alternative to hemodialysis-related intolerance. We report on our experience and that of others with cirrhotic patients with ascites treated by peritoneal dialysis. Hemodynamic tolerance was excellent in all patients and solute and water peritoneal transport increased to above the normal range in almost all cases. Morbidity and mortality were related principally to liver disease and other comorbidities. Peritoneal protein losses, initially high, decreased over time, maintaining serum albumin within the low normal range. The incidence of peritonitis was similar or slightly higher than usual in these patients, with peculiar etiology. The experiences with peritoneal dialysis suggest consideration of this treatment as the first choice for cirrhotic patients with ascites and that need to start dialysis.

Selenium (Se) is a trace element that participates as a cofactor in several enzymes (selenoproteins) which act in the regulation of thyroid hormone metabolism, enzymatic antioxidant defenses and the immune system. Se deficiency has been linked to atherosclerosis-related cardiovascular disease, increased risk of viral infections and even with an increased risk of mortality. Low serum Se levels are a frequent finding in patients with acute kidney injury or chronic kidney disease. The relationship between hyposelenemia and the comorbidities associated with renal disease has not been extensively evaluated. It has been reported that both low serum Se levels and renal insufficiency are associated with an increased risk of coronary heart disease mortality and an increased risk for all-cause mortality in adults older than 35 years. A recent report has suggested that hyposelenemia may contribute to immune dysfunction, increasing the risk of death from infectious disease in hemodialysis patients. Some studies have reported that Se status and immune function improve after oral and intravenous Se supplementation in renal patients, reducing the products of oxidative stress. In summary, although there are intriguing relationships between Se physiology and several derangements and comorbidities associated with acute and chronic kidney disease, only a few studies have analyzed the clinical consequences of hyposelenemia in these patients to date. Available data are encouraging and stimulate interest in further studies to clarify the real extent of Se deficiency and the need for Se supplementation in patients with kidney disease.