Abstract
BackgroundMembranous nephropathy is an important glomerular disease characterized by podocyte injury and proteinuria, but no metabolomics research was reported as yet. Here, we performed a parallel metabolomics study, based on human urine and serum, to comprehensively profile systematic metabolic variations, identify differential metabolites, and understand the pathogenic mechanism of membranous nephropathy.ResultsThere were obvious metabolic distinctions between the membranous nephropathy patients with urine protein lower than 3.5 g/24 h (LUPM) and those higher than 3.5 g/24 h (HUPM) by Partial Least Squares Discriminant Analysis (PLS-DA) model analysis. In total, 26 urine metabolites and 9 serum metabolites were identified to account for such differences, and the majority of metabolites were significantly increased in HUPM patients for both urines and serums. Combining the results of urine with serum, all differential metabolites were classified to 5 classes. This classification helps globally probe the systematic metabolic alterations before and after blood flowing through kidney. Citric acid and 4 amino acids were markedly increased only in the serum samples of HUPM patients, implying more impaired filtration function of kidneys of HUPM patients than LUPM patients. The dicarboxylic acids, phenolic acids, and cholesterol were significantly elevated only in urines of HUPM patients, suggesting more severe oxidative attacks than LUPM patients.ConclusionsParallel metabolomics of urine and serum revealed the systematic metabolic variations associated with LUPM and HUPM patients, where HUPM patients suffered more severe injury of kidney function and oxidative stresses than LUPM patients. This research exhibited a promising application of parallel metabolomics in renal diseases.
Highlights
Membranous nephropathy is an important glomerular disease characterized by podocyte injury and proteinuria, but no metabolomics research was reported as yet
The patients were clinically classified to Low Urine Protein Membranous nephropathy (MN) group (LUPM, urine protein < 3.5 g/24 h) and High Urine Protein MN group (HUPM, urine protein > 3.5 g/24 h)
We proposed a metabolic network associating with the increased oxidative stress during the developing of membranous nephropathy (Figure 4)
Summary
Membranous nephropathy is an important glomerular disease characterized by podocyte injury and proteinuria, but no metabolomics research was reported as yet. Routine clinical chemical measures of renal function based on blood, such as serum creatinine, serum uric acid, albumin, and total protein, are insensitive and laggard for early diagnosis. They elevated significantly only after substantial kidney injury occurs, generally after a loss of two third or greater of nephron functional capacity [4]. The metabolites that are overproduced during MN progression will enter urine space and be secreted into final urine For this reason, urine possibly is an ideal source of test materials to noninvasively characterize the activity of kidney
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