title: Urinary podocyte-associated mRNA profile in various stages of diabetic nephropathy.
abstract: BACKGROUND
  Podocyte injury and subsequent excretion in urine play a crucial role in the pathogenesis and progression of diabetic nephropathy (DN). Quantification of messenger RNA (mRNA) expression in urinary sediment by real-time PCR is emerging as a noninvasive method of screening DN-associated biomarkers. We hypothesized that the urinary mRNA profile of podocyte-associated molecules may provide important clinical insight into the different stages of diabetic nephropathy.
  
  
  METHODS
  DN patients (N = 51) and healthy controls (N = 13) were enrolled in this study. DN patients were divided into a normoalbuminuria group (UAE<30 mg/g, n = 17), a microalbuminuria group (UAE 30∼300 mg/g, n = 15), and a macroalbuminuria group (UAE>300 mg/g, n = 19), according to their urinary albumin excretion (UAE). Relative mRNA abundance of synaptopodin, podocalyxin, CD2-AP, α-actin4, and podocin were quantified, and correlations between target mRNAs and clinical parameters were examined.
  
  
  RESULTS
  The urinary mRNA levels of all genes studied were significantly higher in the DN group compared with controls (p<0.05), and mRNA levels increased with DN progression. Urinary mRNA levels of all target genes positively correlated with both UAE and BUN. The expression of podocalyxin, CD2-AP, α-actin4, and podocin mRNA correlated with serum creatinine (r = 0.457, p = 0.001; r = 0.329, p = 0.01; r = 0.286, p = 0.021; r = 0.357, p = 0.006, respectively). Furthermore, podocalyxin mRNA was found to negatively correlate with eGFR (r = -0.349, p = 0.01).
  
  
  CONCLUSIONS
  The urinary mRNA profiles of synaptopodin, podocalyxin, CD2-AP, α-actin4, and podocin were found to increase with the progression of DN, which suggested that quantification of podocyte-associated molecules will be useful biomarkers of DN.
authors.affiliation: Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, China.
authors.forename: Min
authors.initials: M
authors.lastname: Zheng
authors.forename: Lin-Li
authors.initials: LL
authors.lastname: Lv
authors.forename: Jie
authors.initials: J
authors.lastname: Ni
authors.forename: Hai-Feng
authors.initials: HF
authors.lastname: Ni
authors.forename: Qing
authors.initials: Q
authors.lastname: Li
authors.forename: Kun-Ling
authors.initials: KL
authors.lastname: Ma
authors.forename: Bi-Cheng
authors.initials: BC
authors.lastname: Liu
mesh_terms: D000185:Actinin / Q000235:genetics; D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics; D000328:Adult; D003404:Creatinine / Q000097:blood; D003598:Cytoskeletal Proteins / Q000235:genetics; D003928:Diabetic Nephropathies / Q000097:blood / Q000652:urine*; D005260:Female; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D008840:Microfilament Proteins / Q000235:genetics; D008875:Middle Aged; D050199:Podocytes / Q000378:metabolism*; D012333:RNA, Messenger / Q000097:blood*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012795:Sialoglycoproteins / Q000235:genetics
chemical_list: C111453:ACTN4 protein, human; D048868:Adaptor Proteins, Signal Transducing; C114545:CD2-associated protein; D003598:Cytoskeletal Proteins; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D008840:Microfilament Proteins; C407223:NPHS2 protein; D012333:RNA, Messenger; C503967:SYNPO protein, human; D012795:Sialoglycoproteins; C001643:podocalyxin; D000185:Actinin; D003404:Creatinine