Abstract 5270: Vascular Function and Vascular Inflammation in Polycystic Kidney Disease
Background: Polycystins, which have been localized to vascular smooth muscle cells, may lead to vascular dysfunction and contribute to cardiovascular disease in autosomal dominant polycystic kidney disease (ADPKD). We examined vascular function and vascular inflammation in ADPKD.
Methods: This is an ancillary study to the Halt Progression in PKD Study, which is examining the effect of renin-angiotensin-aldosterone blockade on progression of ADPKD. We used peripheral arterial tonometry to assess augmentation index (AIx), a measure of arterial stiffness and wave reflection, in 52 ADPKD patients with hypertension and glomerular filtration rate (GFR) 25– 60 ml/min/1.73 m2, 50 ADPKD patients with hypertension and GFR >60 ml/min/1.73 m2, and 51 healthy controls. We measured serum levels of soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (VCAM-1), p-selectin, e-selectin, soluble Fas, and Fas ligand (FasL) as markers of vascular inflammation.
Results: AIx, sICAM, p-selectin, and Fas were higher, and FasL was lower in subjects with ADPKD (p<0.05, Table⇓). Adjusting for age, race, height, heart rate, and mean arterial pressure had no effect on group differences in AIx (healthy control = 8%, ADPKD GFR >60 = 21%, ADPKD GFR 25– 60 = 20%). Group means were significantly different even after adjustment for vascular inflammatory markers (healthy control = 3%, ADPKD GFR >60 = 24%, ADPKD GFR 25– 60 = 24%). There were no differences in AIx, sICAM, p-selectin, e-selectin, or FasL between the two ADPKD groups (Table 1⇓, p>0.05).
Conclusion: Vascular dysfunction and vascular inflammation are evident even in early stages of ADPKD with preserved GFR. Further research is needed to examine the relative contributions of genetic aberrations, hypertension, and reduced kidney function to the pathophysiology of vascular dysfunction in ADPKD.