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Low molecular uremic toxin

Dec 30, 2016
P: P retention can inhibit renal 1- alpha hydroxylase activity and 1, 25 (OH) for the synthesis of 2D3, reduce the release of calcium from bone and reduce the calcium levels in the blood, resulting in increased secretion of PTH. Recent studies show that hyperphosphatemia has a direct stimulating effect on parathyroid, high phosphorus can make the parathyroid transforming growth factor alpha (TGF- alpha) increase the expression of parathyroid cell proliferation and stimulation of parathyroid hormone (PTH) secretion. Hyperphosphatemia can induce vascular smooth muscle cell phenotype transformation, which has the characteristics of osteoblasts, and the expression of osteopontin and osteocalcin and promote vascular calcification (the discovery is considered to have "milepost" kind of meaning).
H + and metabolic acidosis: H + is essential for the regulation of acid-base balance and stability of the in vivo environment, and the body's requirement for H + is relatively constant. Metabolic acidosis may occur when H + is produced in excess or in the absence of an obstruction. Patients with uremia and most patients with end-stage renal failure (Pre-ESRD) had metabolic acidosis. The metabolic acidosis in patients with mild to moderate chronic renal failure (GFR>25ml/min) is usually renal tubular acidosis. Metabolic acidosis can cause damage to multiple systems in the body. It can affect the metabolism of protein, calcium and phosphorus metabolism, appetite and digestion, the formation of red blood cells, bone development, muscle function, cardiovascular function, nervous system function, immune function and so on. Therefore, a large number of facts show that excessive capture is one of the important uremic toxins.
Urea and thiocyanate: urea as the major end product of protein metabolism, the molecular structure of CO (NH2), a molecular weight of 60, which contained 46.7% nitrogen (28/60), the serum urea nitrogen determination value equivalent to about half the value of the determination of urea (28/60). In the past, it was thought that the main symptoms of uremia were caused by urea, but later studies showed that the toxicity of urea itself was not very strong. When the body of urea can be transformed into thiocyanate, isothiocyanate molecules by carbamylation is cleared when the renal function damage, urea and its metabolites can not effectively eliminate, accumulate in the body, can lead to fatigue, headache, lethargy, depression, pruritus, nausea and vomiting; Thiocyanate can cause elevated and weak sleepy, diarrhea, intestinal bleeding, hypothermia, coma, thiocyanate inhibition of neutrophil oxide release to a certain extent, which interfere with the function of killing microorganisms. The amino acid carbamoylation of free amino (C-AA), and another normal amino acid (F-AA) combined with carboxyl groups, thus causes difficulties in protein synthesis, which is one of the factors of malnutrition in uremic patients, can also cause some metabolic disorders, and even affect the tissue and organ function (such as the brain cortical function, peripheral nerve dysfunction etc.).
Guanidine guanidine compounds (guanidio: compounds, GCs) after urea substances produced by metabolism of protein, including guanidine, methylguanidine, two methyl guanidine, creatinine, guanidine acetic acid, guanidinosuccinic acid and 1, 3- two benzene guanidine. Methylguanidine increased can cause nausea and vomiting, diarrhea, anemia, impaired glucose tolerance, plasma fibrinogen and cracking activity decreased, the absorption of calcium, reduce gastric and duodenal ulcer and hemorrhage, convulsions and unconsciousness, can also cause pancreatic secretion, red blood cells and lymphocytes of solution, DNA, synthesis Na-K ATP enzyme activity, calcium -ATP activity inhibition and inhibit norepinephrine transport in sympathetic synaptic vesicles, therefore may cause methylguanidine sympathetic nervous system lesions in chronic renal failure. Guanidinosuccinic acid can inhibit platelet factor -3 activity, inhibition of platelet ADP induced structural changes, inhibition of ADP, epinephrine induced secondary irreversible platelet aggregation, platelet and cause changes in the fine structure. Therefore guanidinosuccinic acid may be one of the causes of coagulation disorders in patients with uremia. A recent study found that guanidinosuccinic acid, methyl guanidine and creatinine as a competitive antagonist, acting on the conductor cognition of GABA receptor sites.
Asymmetric two amino acid: asymmetric (ADMA) is an endogenous inhibitor of endothelial nitric oxide synthase (NOS), its molecular weight is 202D. ADMA and its physiologically active stereoisomers, symmetric two arginine (SDMA), are partly excreted by the kidneys. The activity of ADMA can be inhibited by oxidized low density lipoprotein or tumor necrosis factor. ADMA is a potent inhibitor of NO synthesis, and there is a significant correlation between the level of serum ADMA and the thickness of carotid artery, suggesting that ADMA may be one of the markers of atherosclerosis. Advanced glycation end products and end products of lipid oxidation
Oxalic acid: the concentration of oxalic acid in plasma is increased, and it is consistent with the concentration of urea nitrogen. Because of the high concentration of oxalic acid in red blood cells, the whole blood concentration of oxalic acid is higher than that of plasma. Normal oxalate excreted in the urine, blood dialysis can remove the oxalic acid, consistent with the level of plasma levels of ascorbic acid oxalate. According to reports, a large number of pyridoxine hydrochloride can reduce the levels of oxalate. The oxalate solubility is very low, high concentration of oxalate can induce calcium oxalate deposition in soft tissue and urinary calcium oxalate calculi; renal tissue and myocardium is also found in calcium oxalate crystals. It has been reported that in patients with maintenance hemodialysis, calcium oxalate deposition can cause congestive heart failure.
N- is acyl serine aspartic - lysyl - proline (AcSDKP): AcSDKP with low molecular weight substances as part of creatinine, serum AcSDKP levels are elevated in patients with renal failure, it can be found in vivo and in vitro angiotensin-converting enzyme degradation, so the blood level generated by the angiotensin converting enzyme for the degradation and excretion of kidney to decide. Therefore, patients with angiotensin converting enzyme inhibitor treatment of blood AcSDKP was significantly increased, compared with the control group can be increased by 4 times, the concentration of hemodialysis can be reduced by 60%. It has been found that the AcSDKP is a physiological inhibitor of erythropoiesis, it inhibits erythropoiesis by inhibiting hematopoietic stem cells, its accumulation in the blood can cause erythropoietin (EPO) resistance, blood AcSKDP levels in renal failure patients with EPO need is proportional to the amount of.
The activity of vitamin D3 inhibitor: renal failure, decrease the activity of vitamin D3 biological activity, the reason for the activity and concentration of vitamin D3 receptor and reduced the synthesis of uremic toxins can cause vitamin D3 activity declined, for each other, inhibit the vitamin D3 receptor and DNA cellulose in addition, calcium three alcohol synthesis at the transcriptional receptor site is suppressed, and there are obvious calcium three alcohol resistance. Normal kidney function, monocyte CD14 expression induced by calcium three alcohol is increased, while the expression of uremic ultrafiltrate can not only inhibit the basic CD14, CD14 cells can also make calcium three alcohol induced expression was significantly inhibited. Experimental studies have found that uric acid, xanthine, hypoxanthine and other substances with this inhibition.

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