The heart and the vascular tree undergo major structural and functional changes when kidney function declines and renal replacement therapy is required. The many cardiovascular risk factors and adaptive changes the heart undergoes include left ventricular hypertrophy and dilatation with concomitant systolic and diastolic dysfunction. Myocardial fibrosis is the consequence of impaired angio-adaptation, reduced capillary angiogenesis, myocyte-capillary mismatch, and myocardial micro-arteriopathy. The vascular tree can be affected by both atherosclerosis and arteriosclerosis with both lipid rich plaques and abundant media calcification. Development of cardiac and vascular disease is rapid, especially in young patients, and the phenotype resembles all aspects of an accelerated ageing process and latent cardiac failure. The major cause of left ventricular hypertrophy and failure and the most common problem directly affecting myocardial function is fluid overload and, usually, hypertension. In situations of stress, such as intradialytic hypotension and hypoxaemia, the hearts of these patients are more vulnerable to developing cardiac arrest, especially when such episodes occur frequently. As a result, cardiac and vascular mortality are several times higher in dialysis patients than in the general population. Trials investigating one pharmacological intervention (eg, statins) have shown limitations. Pragmatic designs for large trials on cardio-active interventions are mandatory for adequate cardioprotective renal replacement therapy.
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