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Progression of macrovascular disease after transplantation
B J Nankivell1, S G Lau, J R Chapman
1Department of Renal Medicine, University of Sydney, Westmead Hospital, Australia. bn@renal.wh.usyd.edu.au
Insights
Kidney and pancreas transplant recipients showed increased carotid plaque over 10 years. Plaque initiation linked to systemic factors, while progression depended on local arterial changes.
Area of Science:
- Vascular Biology
- Transplantation Medicine
- Diabetology
Background:
- Cardiovascular and cerebrovascular diseases pose significant risks post-kidney transplantation.
- Understanding the progression of vascular disease in uremic, type 1 diabetic patients is crucial.
Purpose of the Study:
- To investigate the natural history of carotid plaque in combined kidney and pancreas transplant recipients.
- To identify risk factors associated with vascular disease progression in this patient cohort.
Main Methods:
- Prospective longitudinal study involving duplex scanning of carotid and lower limb arteries in 82 recipients.
- Data collected before transplantation, at 6 months, and annually for up to 10 years.
- Carotid plaque analysis included type, location, extent, and degree of obstruction, with multivariate evaluation.
Main Results:
- Carotid plaque prevalence rose from 22.5% to 56.6% by 7-10 years post-transplant, particularly in the internal carotid artery (ICA) and common carotid artery.
- Plaque severity, extent, and complexity increased over time, associated with older age, smoking, hyperphosphatemia, hypoalbuminemia, and pre-transplant dialysis duration.
- ICA disease progression was linked to plaque characteristics and reduced renal function, while blood flow was impaired by hypertension and hyperglycemia.
Conclusions:
- Significant increases in carotid vascular wall abnormalities were observed despite transplantation.
- Systemic factors initiated plaque formation, whereas local arterial wall factors predominantly influenced established plaque progression.
Introduction:
Cardiovascular and cerebrovascular disease are major causes of morbidity and mortality after kidney transplantation. The aim of this longitudinal 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 transplant.
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 the internal carotid artery (ICA), external carotid artery, and common carotid 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 scanning, 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 plaque increased, and plaque became more complex and heterogeneous with time after 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<0.05-0.001). The severity of carotid plaque increased in older, hypertensive recipients and was associated with metabolic acidosis and hyperphosphatemia (all P<0.05). Severity of ICA disease correlated with disease in the contralateral ICA (r=0.57, P<0.001) and femoral arteries (r=0.42, P<0.001). Paradoxically, each carotid artery progressed independently of the other. ICA disease severity progressed when heterogenous, calcified, or new plaque was present on scanning, and with reduced renal transplant function (P<0.01-0.001). The mean ICA blood flow remained stable with time but was progressively impaired by hypertension, fasting hyperglycemia, and a lower prednisolone dose (P<0.05). Cerebrovascular events occurred in only four patients and were unrelated to carotid disease, implying relative plaque stability.
Conclusion:
Extensive carotid vascular wall abnormalities increased significantly despite kidney and pancreas transplantation. Initiation of plaque was associated with systemic factors, whereas progression of established plaque was largely influenced by local factors within the arterial wall.