Abstract

The progressive decline of glomerular filtration rate in chronic kidney disease patients is associated with a significant reduction in food intake. Approximately one third of chronic dialysis patients complain of a fair or poor appetite and this is related directly to poor patient outcomes. Appetite regulation involves the gastrointestinal tract (ghrelin as an appetite stimulant, and cholecystokinin, glucagon-like peptide-1, and neuropeptide YY as appetite inhibitors); the adipose tissue with leptin, a potent appetite inhibitor; the vagal system; and the brain, which integrates the stimuli in the hypothalamus area. Satiety relies on the melanocortin receptors with serotonin as the main neurotransmitter and is challenged with hunger peptides, namely, neuropeptide Y and agouti-related peptide. In nondialyzed chronic renal failure patients and in maintenance dialysis patients, anorexia is related mainly to the accumulation of unidentified anorexigenic compounds, inflammatory cytokines, and alterations in appetite regulation, such as amino acid imbalance, which increases the transport of free tryptophan across the blood-brain barrier. This creates a hyperserotoninergic state that is prone to low appetite. Treatment of anorexia involves counseling, starting dialysis treatments in uremic chronic kidney disease patients, increasing the dialysis dose, and possibly using appetite stimulants.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call