To test the hypothesis that PPAR-gamma agonist, rosiglitazone, induces carotid plaque regression in diabetic ESRD patients on maintenance PD via its anti-inflammatory property.
End-stage renal disease (ESRD) patients are at an increased risk of accelerated atherosclerosis and cardiovascular morbidity and mortality. Non-traditional risk factors such as inflammation and insulin resistance have important contributions to accelerated atherosclerosis in ESRD patients receiving long-term peritoneal dialysis (PD). The peroxisome proliferator-activated receptor-g (PPAR-g) is a member of the nuclear receptor family of ligand-dependent transcription factors. Activation of the PPAR-g has been shown in both clinical and experimental studies to have anti-inflammatory and anti-atherosclerotic properties other than insulin-sensitizing effects. Recent study also showed that PPAR-g agonists reduce plaque inflammation by inhibiting the activation of proinflammatory genes responsible for plaque development and growth. Hence, this study aims to examine the effects of PPAR-g activation on the progression of carotid plaque in diabetic ESRD patients receiving long-term PD using high-resolution magnetic resonance imaging (MRI).
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
QUADRUPLE
Enrollment
22
oral Pioglitazone 15mg daily for 12 weeks, then 30mg daily for 36 weeks
Placebo comparator
Queen Mary Hospital and Tung Wah Hospital
Hong Kong, Hong Kong, Hong Kong
Queen Mary Hospital, Tung Wah Hospital
Hong Kong, Hong Kong
Change in carotid plaque volume
Time frame: 12 months
Change in inflammatory markers include C-reactive protein, interleukin-6, adiponectin, metalloproteinases
Time frame: 12 months
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