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Novel Links between the Long Pentraxin 3, Endothelial Dysfunction, and Albuminuria in Early and Advanced Chronic Kidney Disease

Mohamed E. Suliman^*, Mahmut I. Yilmaz^*,, Juan J. Carrero^*, Abdul Rashid Qureshi^*, Mutlu Saglam, Osman M. Ipcioglu, Mujdat Yenicesu, Mengli Tong^*, Olof Heimbürger^*, Peter Barany^*, Anders Alvestrand^*, Bengt Lindholm^*, and Peter Stenvinkel^*

^* Department of Clinical Science, Intervention, and Technology, Karolinska Institutet, Divisions of Renal Medicine and Baxter Novum, Karolinska University Hospital Huddinge, Stockholm, Sweden; and Departments of Nephrology, Radiology, and Biochemistry, Gülhane School of Medicine, Etlik-Ankara, Turkey

Correspondence: Dr. Peter Stenvinkel, Division of Renal Medicine, K56, Karolinska University Hospital at Huddinge, 141 86 Stockholm, Sweden. Phone: +46-8-58582532; Fax: +46-8-7114742; E-mail: peter.stenvinkel{at}ki.se

Background and objectives: Albuminuria and inflammation predict cardiovascular events. Pentraxin 3, an inflammatory mediator produced by, among others, endothelial cells, may have a role in atherogenesis.

Design, setting, participants, & measurements: In 207 Swedish patients with stage 5 chronic kidney disease and 79 Turkish patients with type 2 diabetes and proteinuria and normal renal function, whether serum pentraxin 3 levels are associated with albuminuria and endothelial dysfunction was studied.

Results: Patients with stage 5 chronic kidney disease and a high degree of albuminuria more often had diabetes and higher levels of pentraxin 3, vascular cellular adhesion molecule-1, and blood pressure. Moreover, pentraxin 3 was independently associated with 24-h urinary albumin excretion. In patients with type 2 diabetes, pentraxin 3 was significantly higher than in control subjects. Patients with type 2 diabetes and more proteinuria had higher pentraxin 3, C-reactive protein, glycosylated hemoglobin, insulin, and homeostasis model assessment index as well as lower flow-mediated dilation and serum albumin. Pentraxin 3 was positively correlated with C-reactive protein, homeostasis model assessment index, and carotid intima-media thickness and negatively with flow-mediated dilation. Pentraxin 3 and glomerular filtration rate were independently associated with 24-h urinary protein excretion. Only pentraxin 3 and proteinuria were significantly and independently associated with flow-mediated dilation.

Conclusions: In two different renal cohorts, one of stage 5 chronic kidney disease and one of type 2 diabetes and normal renal function, pentraxin 3 was independently associated with proteinuria. Moreover, both pentraxin 3 and proteinuria were associated with endothelial dysfunction in patients with type 2 diabetes.

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