Correspondence: Kacso Gabriel, Dornei 47 street, 400171 Cluj Napoca, Romania. Tel: + 40 741277206, + 40 742221299. Fax: + 40 264 592202. E-mail: gabi.kacso@gmail.com (Received 21 December 2011; accepted 14 February 2012) ORIGINAL ARTICLE Plasma adiponectin is related to the progression of kidney disease in type 2 diabetes patients INA MARIA KACSO 1 , COSMINA IOANA BONDOR 2 & GABRIEL KACSO 3 Departments of 1 Nephrology, 2 Informatics and Biostatistics, and 3 Oncology, University of Medicine and Pharmacy ‘Iuliu Hatieganu’ Cluj Napoca, Romania 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 evalu- ation, 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 adi- ponectin 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 regres- sion 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 DGFR, but adiponectin inversely (r =- 0.26, p = 0.02) correlated to DUACR. In multiple regression only adiponectin ( p  0.0001) predicted DUACR. 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 D PI between end of study and baseline (r =- 0.43, p  0.0001), and predicted D 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 Introduction Adiponectin, the most abundant adipokine is credited with antiatherogenic, anti-inflammatory and insulin- sensitizing properties. Lower levels of adiponectin are associated with the prevalence and development of type 2 diabetes (T2D), obesity and metabolic syn- drome [1–3] and also with accelerated atherosclerosis and cardiovascular disease [4–7]. Adiponectin is involved in all stages of plaque development, from endothelial dysfunction to plaque rupture, exerting antioxidant activity through AMP-activated kinase- mediated pathways and inhibiting nuclear factor kB- dependent inflammation [8]. The role of adiponectin in kidney disease is a mat- ter of debate. Plasma adiponectin increases with reduced glomerular filtration rate (GFR) [9–12], but also parallels proteinuria and increased urinary adi- ponectin excretion, independently of GFR [13–17], acting as a counter-regulatory anti-inflammatory mechanism directed to mitigate cardio-vascular and renal damage. On the one hand, adiponectin has been shown to exert antiproteinuric and renoprotective effects in experimental models of nondiabetic and dia- betic kidney disease [18,19]. This makes sense, as the kidneys have an enormous endothelial surface and the endothelial dysfunction is known to be an early step in many kidney diseases, including diabetic nephropa- thy. On the other hand, in some studies, increase of this anti-inflammatory cytokine is paradoxically asso- ciated with worse cardiovascular and renal outcome. In order to clarify the potential role of adipon- ectin in the progression of early T2D nephropathy, Scandinavian Journal of Clinical & Laboratory Investigation, 2012; 72: 333–339 ISSN 0036-5513 print/ISSN 1502-7686 online © 2012 Informa Healthcare DOI: 10.3109/00365513.2012.668928