Abstract
Kidney dysfunction leads to disturbed renal metabolic activities and to impaired glomerular filtration, resulting in the retention of toxic solutes affecting all organs of the body. Cardiovascular disease (CVD) and infections are the main causes for the increased occurrence of morbidity and mortality among patients with chronic kidney disease (CKD). Both complications are directly or indirectly linked to a compromised immune defense. The specific coordinated roles of polymorphonuclear leukocytes (PMNLs), monocytes/macrophages, lymphocytes and antigen-presenting cells (APCs) in maintaining an efficient immune response are affected. Their normal response can be impaired, giving rise to infectious diseases or pre-activated/primed, leading to inflammation and consequently to CVD. Whereas the coordinated removal via apoptosis of activated immune cells is crucial for the resolution of inflammation, inappropriately high apoptotic rates lead to a diminished immune response. In uremia, the balance between pro- and anti-inflammatory and between pro- and anti-apoptotic factors is disturbed. This review summarizes the interrelated parameters interfering with the immune response in uremia, with a special focus on the non-specific immune response and the role of uremic toxins.
Highlights
Magnitude of the ProblemThe development of chronic kidney disease (CKD) is associated with a significant increase in all-cause mortality [1]
Kidney dysfunction leads to disturbed renal metabolic activities and to impaired glomerular filtration, resulting in the retention of toxic solutes affecting all organs of the body
A diminished immune defense contributes to the high prevalence of infections, whereas pre-activation and priming of immune cells lead to inflammation and to Cardiovascular disease (CVD)
Summary
The development of CKD is associated with a significant increase in all-cause mortality [1]. The main factors responsible for the increased risk of morbidity and mortality in patients with CKD are CVD and infections [3,4] Both complications are linked to a disturbed immune response (Figure 1). Deranged functions of PMNLs contribute to the increased risk of bacterial infections and represent a main cause for the enhanced risk of morbidity and mortality among CKD patients [6]. Dialysis patients have higher annual mortality rates caused by sepsis compared with the general population, even after stratification for age, race and diabetes mellitus [9]. This graded risk of cardiovascular mortality with decreasing GFR increases distinctly at an estimated GFR < 45 mL/min/1.73 m2 [15]
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