Novel links between the long pentraxin 3, endothelial dysfunction, and albuminuria in early and advanced chronic kidney disease.
OBJECTIVE
Albuminuria and inflammation predict cardiovascular events. Pentraxin 3, an inflammatory mediator produced by, among others, endothelial cells, may have a role in atherogenesis.


METHODS
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.
Suliman
Mohamed E
ME
Department of Clinical Science, Intervention, and Technology, Karolinska Institutet, Divisions of Renal Medicine and Baxter Novum, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Yilmaz
Mahmut I
MI
Carrero
Juan J
JJ
Qureshi
Abdul Rashid
AR
Saglam
Mutlu
M
Ipcioglu
Osman M
OM
Yenicesu
Mujdat
M
Tong
Mengli
M
Heimbürger
Olof
O
Barany
Peter
P
Alvestrand
Anders
A
Lindholm
Bengt
B
Stenvinkel
Peter
P
D000328:Adult; D000419:Albuminuria / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D001794:Blood Pressure; D002097:C-Reactive Protein / Q000378:metabolism*; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D002908:Chronic Disease; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D005919:Glomerular Filtration Rate; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood; D007674:Kidney Diseases / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D012720:Severity of Illness Index; D013548:Sweden; D014421:Turkey; D014463:Ultrasonography; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014664:Vasodilation; D000099153:Pentraxins
D002097:C-Reactive Protein; D006442:Glycated Hemoglobin; D007328:Insulin; D000683:Serum Amyloid P-Component; D019010:Vascular Cell Adhesion Molecule-1; D000099153:Pentraxins