Chronic kidney disease and peritoneal dialysis induced inflammation
Abstract
Cardiovascular diseases are the main cause of mortality and morbidity in people with CKD receiving peritoneal dialysis. This increased risk is likely brought about by the high inflammatory burden associated to CKD and to PD therapy. How systemic and local inflammation influences the development and progression of cardiovascular disease in this context is discussed in Chapter 1 and the current gaps in knowledge are explored. The main aim of this thesis was to understand how and to what extent inflammation secondary to CKD and peritoneal dialysis is driving the development of cardiovascular disease. In Chapter 2 we developed and characterised a new model. We combined a 5/6ths nephrectomy, peritoneal dialysis fluid exposure and a high-cholesterol diet into a new model of atherosclerosis. We found PD-fluid specifically accelerated and aggravated the plaque phenotype and progression. These changes were accompanied by rampant vascular and systemic T-cell inflammation, most notably increases in T-cells bearing the vascular homing marker CX3CR1. These data suggest an essential role for T-cell inflammation, in particular vascular homing T-cells. In Chapter 3 we demonstrated that anti-inflammatory therapy, in the form of anti-galectin-2 nanobodies, was able to ameliorate the progression of existing atherosclerosis in ApoE-/- mice by polarising macrophages towards a classically anti-inflammatory “M2” like phenotype. Importantly these nanobodies were also previously described to promote…
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