A literature review on uraemic encephalopathy

Abstract

Uraemic encephalopathy is an organic brain disorder. It is a state of global cerebral dysfunction, often in the absence of primary structural brain disease. It develops in patients with either acute kidney injury or chronic kidney disease, usually when the estimated glomerular filtration rate (eGFR) falls and remains below 15mL/min.
Numerous organic substances accumulate in the presence of renal failure acting as uraemic neurotoxins. There has been no single metabolite identified as the sole cause of uraemia. Possible organic compounds associated with uraemic encephalopathy are urea, guanidino compounds, uric acid, hippuric acid, various amino acids, polypeptides, polyamines, phenols and conjugates of phenol, phenolic and indolic acids, acetone, glucuronic acid, carnitine, myoinositol, sulphates and phosphates. Despite this numerous organic compounds, urea has been used as a marker of uraemic retention and removal for several years.
The clinical presentation of uraemic encephalopathy appears to correlate with the rate of development of renal failure. It is more pronounced and rapidly developing in patients with acute kidney injury compared to patients having chronic kidney disease. Uraemic encephalopathy usually presents with alterations in mental status fluctuating from mild sensorial clouding to delirium and coma. Other common findings include apathy, fatigue, irritability and inattentiveness usually occurring early while confusion, disturbances of sensory perception, hallucinations and stupor appear later.
This condition is managed by dialysis and dietary modification. Definitive management in end – stage renal disease will be kidney transplantation.

Materials and Methods: The materials used in this review article come from studies and publications on uremic encephalopathy from PubMed, Google Scholar Science Direct, Biomedcentral and Medline databases.