Table 1.

Functional disturbances caused by selected uremic toxins.

Uremic toxin	Functional disturbance
LMW Solutes
Phenylacetic acid (PAA)	Macrophages: inducible nitric oxide synthase ↓ [106];
	PMNLs: oxidative burst, phagocytosis and integrin expression ↑; apoptosis ↓ [49]
Dinucleoside polyphosphates	Leukocytes: oxidative burst ↑ [107].
Guanidino compounds	Monocytes/macrophages: pro- and anti-inflammatory [108,109,110]
Indoxyl sulfate	Endothel: E-selectin ↑ [111]
P-cresyl sulfate	Leukocytes: basal oxidative burst ↑ [112]
Homocysteine (Hcy)	ICAM-1 ↑ [113]; damage of DNA [114] and proteins [115]
Methylglyoxal (MGO)	PMNLs: apoptosis ↑ [116], oxidative burst ↑ [117];
	Monocytes: apoptosis ↑ [118]
Middle Molecules, Proteins
Immunoglobulin light chains (IgLCs)	PMNLs: chemotaxis ↓, glucose uptake stimulation ↓, glucose uptake basal ↑ [119]; apoptosis ↓ [47]
Retinol binding protein (RBP)	PMNLs: chemotaxis ↓, oxidative burst ↓, apoptosis ↓ [120]
Leptin	PMNLs: chemotaxis ↓, oxidative burst ↓ [121]
Resistin	PMNLs: chemotaxis ↓, oxidative burst ↓ [122]
Tamm-Horsfall protein (THP)	PMNLs: (high concentrations) apoptosis ↓, chemotaxis ↓, phagocytosis ↑; (low concentrations) chemotaxis ↑ [123]
High-density lipoprotein (HDL)	Loss of anti-inflammatory properties in uremia [124,125]
Protein Modifications
Glucose-modified proteins	PMNLs: chemotaxis ↑, glucose uptake ↑, apoptosis ↑ [48]
AGE-modified albumin	Leukocytes: activating, pro- atherogenic [126]
AGEs	Macrophages: TNF and IL-1 secretion ↑ [127]
	Monocytes: Chemotaxis ↑ [128]
Glycated collagen	PMNLs: Adhesion ↑ [129]
Advanced oxidation protein products (AOPPs)	PMNLs and monocytes: oxidative burst ↑ [130]
Oxidized low-density lipoproteins (oxLDLs)	Macrophage activation [131];
	PMNLs and eosinophils: chemotaxis ↑, degranulation ↑ [132];
	Regulatory T cells: proteasome activity ↓ → cell cycle arrest and apoptosis [133]
Homocysteinylated albumin	Monocytes: adhesion ↑[134]