Association of Fetuin-A With Kidney Disease; a Review on Current Concepts and New Data Publisher



Akbari M¹ ; Nayeri H¹ ; Nasri H² Show Affiliations
Source: Journal of Nephropharmacology Published:2019

Abstract

Fetuin-A (α2Heremans-Schmid glycoprotein) is a glycoprotein which is synthesized in the liver and secreted into the bloodstream. It belongs to a large group of binding proteins mediating the transport and availability of a wide variety of cargo substances in the bloodstream. The aim of this study is to summarize the available results of studies on the association of fetuin-A with chronic kidney disease and end-stage renal disease, type 2 diabetes, non-alcoholic fatty liver, and yield the end results. The databases including PubMed, Google Scholar, Scopus, and Science-Direct were searched with the purpose of finding the related studies. The articles were assessed in terms of repeatability of title, type of study, population, study variables and the quality of reporting. Finally, 37 articles, which were published between the years 2002 and 2018, were selected to be overviewed completely. The studies showed that fetuin-A can function as a protective inhibitor of vascular calcification in patients with chronic kidney disease and end-stage renal disease, and is reduced during acute inflammation. The deficiency of this protein is associated with an increase in the morbidity and mortality of patients with cardiovascular diseases. Fetuin-A can be useful as a vascular disease marker in patients with type 2 diabetes. In fact, it is an independent predictor of type 2 diabetes due to its high concentration in insulin resistance. Fetuin-A is a good indicator of liver cells function and its level will be increased in non-alcoholic fatty liver disease. Fetuin-A, as a multi-functional protein, performs many tasks. However, studies in this area are very limited and based on its multiple and complex functions, further studies are recommended. © 2019 The Author(s); Published by Society of Diabetic Nephropathy Prevention. T.