Changes in the inflammatory markers with advancing stages of diabetic nephropathy and the role of pentraxin-3

Abstract

Background: Immunological and inflammatory mechanisms have been shown to have role in both the development and progression of diabetic nephropathy (DNP). There is need for more specific markers for inflammation as the ones commonly used are influenced by many factors. Pentraxin-3 (PTX-3) seems to be a potential candidate. We aimed in our study to evaluate the changes of PTX-3 levels in different stages of DNP and its relationship with other inflammatory markers.Methods: This is a cross sectional study in which patients with DNP at different stages were involved. Patient were divided into three groups according to estimated glomerular filtration rate (eGFR), microalbuminuria and proteinuria levels: Group-1: eGFR >60 mL/min and microalbuminuria, Group-2: eGFR >60 mL/min and macroalbuminuria, Group-3: eGFR <60 mL/min and macroalbuminuria. Besides the routine biochemical parameters, levels of PTX-3, high sensitivity C-reactive protein (hsCRP), interleukin (IL)-1 and tumor necrosis factor (TNF)-a was measured. Groups were compared with each other regarding the study parameters and correlation of PTX-3 with other markers was evaluated. Results: The mean PTX-3 level in Group-2 (0.94 ± 0.26 ng/mL) and -3 (1.35 ± 1.55 ng/mL) were higher than in Group-1 (0.81 ± 0.25 ng/mL) (p ¼ 0.009 and p ¼ 0.012). There was a significant correlation of PTX-3 with proteinuria (r ¼ 0.266, p ¼ 0.016), microalbuminuria (r ¼ 0.304, p ¼ 0.014) and hypoalbuminemia (r ¼ 0.197, p ¼ 0.043). PTX-3 was not correlated with other markers of inflammation (IL-1, TNF-a and hsCRP) and diabetic metabolic parameters (hbA1c, C-peptide, insulin and HOMA-IR). PTX-3, IL-1 and TNF-a levels increased with the advancing stage of DNP while hsCRP level did not change. Conclusion: PTX-3 that increases similar to other markers of inflammation (IL-1, TNF-a) is a better inflammatory marker than hsCRP. Furthermore, there is a relationship between PTX-3 and proteinuria independent from eGFR.

The renoprotective effect and safety of a DPP-4 inhibitor, sitagliptin, at a small dose in type 2 diabetic patients with a renal dysfunction when changed from other DPP-4 inhibitors: REAL trial

“…Changes in eGFR and eGFRcys were not statistically significant during the study by repeated ANOVA Changes in UACR, Urinary β2-microglobulin, Urinary collagen IV, L-FABP, and U-8 isoprotane were not statistically significant during the study by Friedman test and is independent of eGFR [19]. In the present study, no significant changes have been noted in the various biomarkers as mentioned above after changing the drugs.…”

Long Non-Coding RNA NEAT1 Regulates Pyroptosis in Diabetic Nephropathy via Mediating the miR-34c/NLRP3 Axis

“…Indeed, the accumulation of inflammatory cells in the kidneys has been shown in both DN patients and mouse models of DN while the extent of accumulation is associated with the progress of renal dysfunction [29-31]. Moreover, local and circulating levels of proinflammatory cytokines are increased in humans and animals with DN [32, 33]. However, the cause of inflammation in DN is still unclear.…”

UroPathogenic Escherichia coli (UPEC) Infections: Virulence Factors, Bladder Responses, Antibiotic, and Non-antibiotic Antimicrobial Strategies

“…Pathogen sensing by TLR4 induces the production of various soluble factors which are secreted by BECs, including antimicrobial peptides (AMP, such as cathelicidin and β-defensin 1; Sun et al, 2013 ; Chromek, 2015 ), antimicrobial proteins [such as pentraxin 3 (PTX3); (Uzun et al, 2016 )] and chemokines [such as CXC-chemokine ligand 1 (CXCL1) and CC-chemokine ligand 5 (CCR5); Schiwon et al, 2014 ; Figure 3E ]. Attachment to the urothelium or bacterial lysis are inhibited by these antimicrobial peptides, which are also induced when bacteria succeed to attach to the urothelium (Spencer et al, 2014 ).…”