Progression of macrovascular disease after transplantation

Introduction. Cardiovascular and cerebrovascular disease are major causes o f morbidity and mortality after kidney transplantation. Tbe aim of this lon gitudinal study was to examine the natural history of carotid plaque and to determine risk factors for the progression of vascular disease in uremic, type 1 diabetic patients who received a combined kidney and pancreas transp lant. Methods. Carotid artery (n=765) and lower limb vascular duplex scanning (n= 656) were prospectively undertaken in 82 recipients before transplantation, at 6 months, and then at annual intervals for up to 10 years. Plaque in th e internal carotid artery (ICA), external carotid artery, and common caroti d artery was classified by type, location, extent, and degree of functional obstruction, and evaluated using multivariate analysis. Results. Carotid plaque was present in 22.5% of patients at, initial scanni ng, but increased to 56.6% by 7-10 years after transplantation, especially in the ICA and common carotid artery. Both the severity and extent of plaqu e increased, and plaque became more complex and heterogeneous with time aft er transplantation (P<0.001). Carotid plaque was associated with older age, current cigarette smoking, hyperphosphatemia, hypoalbuminemia, duration of pretransplantation dialysis, and presence of lower limb plaque (P<0.05-0.0 01). The severity of carotid plaque increased in older, hypertensive recipi ents and was associated with metabolic acidosis and hyperphosphatemia (all P<0.05). Severity of ICA disease correlated with disease in the contralater al ICA (r=0.57, P<0.001) and femoral arteries (r=0.42, P<0.001), Paradoxica lly, each carotid artery progressed independently of the other. ICA disease severity progressed when heterogenous, calcified, or new plaque was presen t on scanning, and with reduced renal transplant function (P<0.01-0.001). T he mean ICA. blood flow remained stable with time but was progressively imp aired by hypertension, fasting hyperglycemia, and a lower prednisolone dose (P<0.05), Cerebrovascular events occurred in only four patients and were u nrelated to carotid disease, implying relative plaque stability. Conclusion. Extensive carotid vascular wall abnormalities increased signifi cantly despite kidney and pancreas transplantation. Initiation of plaque wa s associated with systemic factors, whereas progression of established plaq ue was largely influenced by local factors within the arterial wall.