Abstract
A high level of uric acid may cause hyperuricemia, which further develops into gout, eventually leading to chronic kidney disease. However, the pathogenic mechanism remains largely unknown. To investigate the cause and block the transformation of hyperuricemia to related diseases, it is important to discover the alterations in protein levels between gout patients and non-gout individuals. To date, human blood plasma is still the predominant matrices for clinical analysis. Due to the high abundance, the proteins of plasma samples have strong shielding effects on low abundance proteins, thus, the information on low abundance protein expression is always masked, while the low abundance proteins of human plasma are often of great significance for the diagnosis and treatment of diseases. Therefore, it is very important to separate and analyze the plasma proteins. High-performance liquid chromatography (LC) tandem mass spectrometry (MS)-based proteomics has been developed as a powerful tool to investigate changes in the human plasma proteome. Here, we used LC-MS/MS to detect the differential proteins in the plasmas from simple gout patients, gout with kidney damage patients, and non-gout individuals. We identified 32 obviously differential proteins between non-gout and gout subjects and 10 differential proteins between simple gout and gout with kidney damage patients. These differential proteins were further analyzed to characterize their localization and functions. Additionally, the correlation analysis showed multiple relationships between the abnormal plasma proteins and clinical biochemical indexes, particularly for the immune-inflammatory response proteins. Furthermore, inflammation factors gelsolin (GSN) were confirmed. Our results offer a view of plasma proteins for studying biomarkers of gout patients.
Highlights
Uric acid, a weak diprotic acid, is the terminal product of purine metabolism in humans [1]
The fasted overnight blood samples were collected from 8 non-gout subjects as the normal control group (NC), 8 male gout patients alone (G), and 8 male gout patients combined with renal injury (GN)
To obtain the profile of proteins in the gout study, we took plasma samples from 16 patients with gout and from 8 normal people, and the formed three groups of samples
Summary
A weak diprotic acid, is the terminal product of purine metabolism in humans [1]. Emerging evidence indicates that hyperuricemia is an independent risk factor for chronic kidney disease (CKD) [2,3]. It is often stated that the prevalence of hyperuricemia and gout has increased in recent years [4,5,6]. The prevalence of gout and hyperuricemia has increased in developed countries over the past two decades and research into the area has become progressively more active. According to a 2014 study, the adjusted prevalence of hyperuricemia among Chinese adults in 2009–2010 was about 8.4–13.3% [7]. Many epidemiological studies have shown that hyperuricemia and gout are associated with the development of hypertension, cardiovascular disease, chronic kidney disease, and so on [2]
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