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Protein bound uremic toxin
At present, there can be used for quantitative analysis of 25 kinds of protein with toxoid, including two oxygen methyl resorcinol, hydroquinone, phenol, p-cresol, 3- deoxy glucose aldehyde, fructose lysine methyl aldehyde, B two, B two aldehyde, carboxymethyl lysine, pentosidine, 3 acetic acid urea indole, dog, dog urine quinolinic acid, kynurenic acid, melatonin, quinolinic acid, two tetramethylene amine, spermidine, spermine, leptin, retinol binding protein, hippuric acid, homocysteine, 3- -4- a -5- C - carboxyl group furan ketovaleric acid etc..
Phenols and phenolic acids, phenolic hydroxyl benzoic acid cresol, including 4-, 4- carboxyl benzoic acid two carboxyl benzoic acid. Phenolic acid benzoic acid by ammonia or tyrosine by oxidation and decarboxylation, deamination, some of which are generated in the intestinal bacterial enzyme. Phenolic compounds are bound to glucuronic acid or sulfuric acid in liver. Inhibition of phenolic compounds and the central nervous system in patients with uremia; high concentration of phenol can inhibit Na+-K+ enzymes such as ATP enzyme, -ATP enzyme, calcium magnesium -ATP can also inhibit the enzyme activity caused by liver and brain cell activity, resorcinol acid may also interfere with platelet factor -3A, and inhibit platelet aggregation secondary.
Indoxyl sulfate from indole (Indoles) metabolism in the liver and its toxicity to inhibit drug and protein binding, accelerated glomerulosclerosis, inhibition of thyroxine (T4) and iodine, and the relativity of uremic patients with hypothyroidism have a certain relationship. It has a delayed effect on the repair of damaged vascular endothelial cells. The accumulation of indole sulfate in the brain is related to the abnormal function of the nervous system.
Polyamines polyamines are metabolites of amino acids, including spermine, spermidine, putrescine, cadaverine amine. Increased polyamines can cause anorexia, nausea, vomiting, proteinuria. Blood polyamines increase is one of the main reasons of anemia in uremic patients, possibly by interfering with erythropoietin receptor, has inhibitory effect on the generation of red blood cells, or direct damage to the generation of red blood cells; red blood cells increased polyamine levels, but also one of the reasons for red blood cell life, autolysis; high concentration of polyamines the blood red blood cell colony forming unit hypolasia. Polyamines can make uremia decreased when red blood cells showed sensitive ATP activity from intracellular sodium ion transfer to the outside of the cell decreased, the intracellular sodium concentration increased; also has inhibitory effect on Na+-K+ enzyme and -ATP enzyme of magnesium ATP. Polyamines can enhance the permeability of microcirculation. Pericardial effusion, pulmonary edema, cerebral edema, and intractable renal ascites in patients with uremia may be related to the increased capillary permeability caused by hyperlipidemia.
Advanced glycation end products (AGEs) and lipid oxidation end products (ALEs) in uremic patients: plasma protein and collagen in AGEs, such as pentoside N sigma carboxymethyl lysine (CML) increased significantly; the plasma ALEs such as malonic acid acetaldehyde lysine (MDA-lyS) level was also increased the. AGEs and ALEs with the accumulation of glucose and triglyceride level are not consistent, they mainly come from the precursor plasma molecules are small, active, high concentration of AGEs and ALEs, namely the carbonyl compounds, therefore, uremia can also be set as a "carbonyl overload" or "carbonyl stress". While AGEs and ALEs should be referred to as the end product of carbonyl stress. Carbonyl stress is associated with an increase in carbohydrate and lipid oxidation and non oxidative responses, as well as a reduction in renal clearance of reactive carbonyl compounds. In addition, a large number of enzymatic and non enzymatic channels can also be toxic to reactive carbonyl compounds, uremia, the efficiency of these channels is reduced, but also lead to the increase of reactive carbonyl compounds. With more than 90% pentoside and CML and albumin, the remaining part of the free form of regular hemodialysis and peritoneal membrane can only remove free form, no effect on serum total AGEs concentrations and high flux dialysis membrane is likely to decrease plasma levels. The damage of carbonyl stress can cause multiple systems with a variety of organizations, resulting in long-term complications of chronic renal failure and dialysis; ALEs and AGEs of proteins and peptides modified, is one of the main ways to cause tissue injury.
Hippuric acid (hippuric acid, HA): Patients with chronic renal insufficiency due to active transport, reduced renal blood flow and uremic toxins inhibit renal tubular excretion of HA in urine, to reduce plasma HA concentration increased. When the concentration of HA was 2mg/dl, the red blood cell line could be significantly inhibited, and HA could affect the activity of glucose tolerance and the activity of platelet cyclooxygenase. It was found that the HA of uremic dialysis patients had a good correlation with residual renal function, so HA may be one of the best markers to reflect the residual renal function.
3- -4- a -5- C -2 furan carboxylic acid (CMPF): CMPF is one of the furan fatty acid, it has a strong lipophilic structure, can inhibit the renal uptake of hippuric acid (PAH), and reduce renal drug excretion and metabolism of drugs and endogenous organic acids produced by PAH, which clear channel therefore, removal of PAH can inhibit CMPF. Iodine removal CMPF can inhibit liver glutathione -S- converting enzyme, inhibition of mitochondrial respiration and thyroxine 4; oxidation inhibition of adenosine two phosphate stimulation Nicole amide adenine dinucleotide substrate connection. There is evidence that CMPF is consistent with its neuropathy.
Leptin (Leptin): increased leptin can lead to decreased appetite, reduced nutrient intake
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