Plasma adiponectin is related to the progression of kidney disease in type 2 diabetes patients

Abstract

Background. Adiponectin, an anti-inflammatory and insulin-sensitizing cytokine, has been shown to reduce proteinuria and glomerulosclerosis in experimental models. We assessed the relationship of plasma adiponectin to the progression of kidney disease in type 2 diabetes (T2D) patients. Methods. T2D nonnephrotic patients with glomerular filtration rate (GFR) >30 ml/min and without acute cardiovascular/inflammatory conditions were included. Laboratory standard evaluation, urinary albumin/creatinine ratio (UACR), total plasma adiponectin, and CRP (C-reactive protein) were determined at inclusion and the end of study. Results. Eighty-six patients (62.79% male) were followed up for 20.53±5.46 months. Baseline GFR was 72.85±26.29 ml/min and UACR was 20.53 (interquartile range 6.82–86.39) mg/g. At baseline adiponectin was significantly correlated to UACR (r =0.40, p =0.0001), HDL cholesterol (r =0.30, p =0.005), GFR (r =− 0.23, P =0.04), body mass index (BMI) (r =− 0.26, P =0.02) and waist circumference (r =−0.27, p =0.01). In multiple regression UACR (p =0.0003) and BMI (p =0.03) were significantly related to baseline adiponectin. The progression of kidney disease was estimated as the difference (D) between end and baseline UACR/month and between end and baseline GFR/month. None of the baseline parameters correlated to ΔGFR, but adiponectin inversely (r =− 0.26, p =0.02) correlated to ΔUACR. In multiple regression only adiponectin (p <0.0001) predicted ΔUACR. A computed progression index (PI) resulting from a linear combination of GFR and UACR was also used to assess progression. Baseline adiponectin was significantly correlated to ΔPI between end of study and baseline (r =− 0.43, p <0.0001), and predicted Δ PI in multiple regression (p =0.009). Conclusion. Low plasma adiponectin predicts progression of kidney disease in T2D patients.

Key Words::

• Adipokines
• albuminuria
• diabetic nephropathies
• disease progression
• inflammation

Acknowledgements

This work was funded by a CNCSIS Romania Idei 1167/2008 grant. We acknowledge Prof. Hancu ND and Prof. Gherman Caprioara Mirela's help and support. We thank Mrs Lenghel Alina Ramona, for her assistance in the collection of data.

Declaration of interest: The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.