09 July 2004
During the past few years, it has become increasingly evident that residual renal function (RRF) is an important and independent predictor of poor outcome in patients with chronic kidney disease (CKD). Although the causes of this observation are not fully understood, it appears that the loss of RRF impairs both fluid removal and clearance of solutes, which in turn leads to uremic toxicity and increased morbidity and mortality. There is increasing evidence that patients with CKD develop signs of fluid overload already in the early phases of the disease, and this may be a stimulus for inflammatory activation. Recently, an inflammatory component was identified in uremic atherosclerotic and non-atherosclerotic cardiovascular disease (CVD), which have been consistently associated with poor clinical outcome in patients with CKD. Signs of systemic inflammation occur in parallel to the impairment in renal function, and the pathophysiology is most likely multifactorial, including a decrease in cytokine clearance, advanced glycation end-product accumulation, oxidative stress, and principal fluid overload. Additionally, inflammation seems to be a predictor of accelerated loss of renal function. In this article, we discuss the evidence showing that patients with CKD generally have fluid overload, the mechanisms by which impaired renal function may lead to a chronic inflammatory state, and the available information linking fluid overload to accelerated loss of renal function and CVD through inflammation. Inflammation may lead to the development of complications of CKD, in particular CVD, but on the other hand may also lead to a faster progression of renal disease. Strategies aiming to reduce fluid overload may be useful to reduce cardiovascular morbidity and mortality, but also preserve RRF.