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Review
. 2012 Oct 24;4(11):962-90.
doi: 10.3390/toxins4110962.

Immune dysfunction in uremia—an update

Gerald Cohen  1 , Walter H Hörl
Affiliations
Review

Immune dysfunction in uremia—an update

Gerald Cohen et al. Toxins (Basel). .

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.

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Figures

Figure 1
Figure 1
Immune dysfunction and risk factors in chronic kidney disease.
Figure 2
Figure 2
Different activation states and conditions influencing leukocyte function upon stimulation.
Figure 3
Figure 3
Kidney failure leads to disturbed renal metabolic activities and to impaired glomerular filtration and/or tubular secretion/reabsorption.
Figure 4
Figure 4
Different uremic toxins may exert antagonistic effects leading to infection and inflammation.
See this image and copyright information in PMC

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