P1042CHEMERIN, INFLAMMATION AND DIABETIC KIDNEY DISEASE PROGRESSION IN PATENTS WITH TYPE 2 DIABETES MELLITUS
Authors: El-Tahir Fatima , Mohamed Ali Moustafa Shendi , Elgohary Marwan , Esh Asmaa Mohammed , Ghorab Adel 
Published: June 2020

Background and Aims

Diabetic kidney disease (DKD) is the leading cause of end-stage renal diseases worldwide. The development of DKD includes immunologic and inflammatory mechanisms which involve activation of the innate immune system and participation of inflammatory cytokines such as tumor necrosis factor (TNF)-α. Chemerin is an adipokine that has been suggested to be related to inflammation and has been correlated with the development of diabetic complications.We aimed to explore the potential links between chemerin, inflammation and the development of DKD in patients with type 2 diabetes mellitus (DM).

Method

The study population included 94 subjects: 84 patients with type 2 DM (89.4%), classified into 3 groups according to the 24 hr urinary albumin, and 10 normoalbuminuric non-diabetic controls (10.6%). Demographic, clinical and analytical data, and chemerin and TNF-α levels were collected.

Results

A total of 84 diabetic patients were enrolled, 32 males (38.1%) and 52 females (61.9%), mean age 57.9±10.7 years. They were divided into 3 groups: 14 with normalbuminuria, 27 with microalbuminuria, and 43 with macroalbuminuria (24 h urinary albumin &lt;30, 30-300 and &gt;300 mg/dl respectively). Chemerin levels increased significantly with the rise in albuminuria (control: 21.3 (10.8 –180), normoalbuminuria: 794 (556.9-1066), microalbuminura: 1155.5 (718 – 1877) and macroalbuminuria: 1619 (705 – 8067) ng/ml; p&lt; 0.001, Kruskal Wallis test), yet with no significant difference between the control and normoalbuminuria groups. Serum TNF-α was significantly elevated in macroalbuminuria compared to control groups (p=0.017) with no significant difference between normoalbuminuria, microalbuminuria and macroalbumenuria groups (control: 77.85 (59 – 124.7), normoalbuminuria: 85.15 (59-146), microalbumenuria: 89 (68 – 180) and macroalbuminuria: 100 (66 – 556) pg/ml) (Figure). Among the diabetics, a significant association was evident between serum chemerin and serum TNF-α (r= 0.84; p&lt;0.001). Both biomarkers were significantly associated with the inflammatory markers ESR and CRP, serum creatinine, BUN, 24 hour urine albumin, HbA1c, and diabetes duration and negatively with eGFR and serum albumin (p&lt;0.05). On linear stepwise regression analysis, chemerin was significantly associated with TNF-α (unstandardized β 9.954, p&lt;0.001) and ESR (unstandardized β 19.596, p&lt;0.001); and TNF-α was significantly correlated with chemerin (unstandardized β 0.059, p&lt;0.001), 24 hour urine albumin (unstandardized β 0.004, p&lt;0.001) and HbA1c (unstandardized β -13.699, p=0.014).

Conclusion

Chemerin increased progressively with the rise in albuminuria, and was associated with the inflammatory milieu in patients with DKD, given the significant association with the inflammatory markers TNF-α and ESR. TNF-α, as surrogate of inflammation, was strongly associated with albuminuria. As such, our results suggest a potential role of Chemerin and TNF-α in the development and progressions of DKD. Larger studies are warranted to further explore the potential links between chemerin, inflammation and DKD.