How to reduce creatinine and urea nitrogen?

Creatinine (English: Creatinine), also known as creatinine, creatine and creatine phosphate metabolism end products, which is mainly generated by non-enzymatic reactions in muscle creatine phosphate. Normal adults, the daily amount of creatinine produced is constant, and the amount of creatinine produced is proportional to the amount of muscle, and therefore the value in general little men than women. Regular exercise muscle and non-vegetarians value is higher. Generating a certain amount of creatinine, but not after the filtering tubular reabsorption. It reflects the excretion of creatinine levels in blood and glomerular filtration rate, which is the function of the kidneys. When severe kidney disease, the creatinine excretion is blocked, blood creatinine levels increased. Determination of creatinine in the blood can be known whether there is severe renal function impairment, creatinine higher the value, the greater the kidney disorder; blood creatinine, but only when there is a serious obstacle to the kidney will be significantly improved, not as early renal disease indicators. Generally normal to: Men 0.7 ~ 1.2 mg / dL (60 ~ 110 μmol / L), F 0.5 ~ 1.0 mg / dL (45 ~ 90 μmol / L), the under-five 0.3 ~ 0.5mg/dl.
Blood urea nitrogen urea nitrogen is the main end-product of human protein metabolism. Deamination of amino acids to generate NH3, and C02, both the synthesis of urea in the liver, per gram of protein metabolism urea 0.3g. Urea nitrogen content of 28/60, almost half. Renal excretion of urea is usually the main organ of urea from the glomerular filtration may be reabsorbed in the tubules of each segment, but within the renal tubular reabsorption of urine flow rate, the faster the less, that reached a maximum clearance. And serum creatinine, as in early renal dysfunction, blood urea nitrogen in the normal range. When the glomerular filtration rate drops to below 50% of normal, blood urea nitrogen concentration was increased rapidly. Under normal conditions, blood urea nitrogen and creatinine ratio (BUN / Scr) value of about 10, high-protein diet, high catabolic state, water shortages, renal ischemia, hypovolemia, and some acute glomerulonephritis, are The ratio can increase, even up to 20 to 30; while low-protein diet, liver disease often makes ratio decreased, this time called low azotemia.
BUN to fasting normal adults 3.2-7.1mmol / L (9-20mg/d1). Variety of renal parenchymal lesions, such as glomerulonephritis, interstitial nephritis, acute and chronic renal failure, renal space-occupying lesions and destructive can make blood urea nitrogen increased. Multi-renal factors may also cause elevated blood urea nitrogen, one can rule out uremia diagnostic indicators such as the kidney and external factors, BUN), 21.4mmol / L (60mg/d1) is.
More vulnerable to the effects of diet, renal blood flow, if protein degradation factors - infections, intestinal bleeding, elevated blood urea nitrogen, which will enable hyperthyroidism. Glomerular filtration rate decreased to the normal 1/2 ~ 1/3, urea nitrogen gradually increased, the ratio of blood urea nitrogen and serum creatinine under normal circumstances is 10.1, the ratio increased due to a gastrointestinal hemorrhage , hemolysis, cardiac dysfunction and tissue breakdown enhancement (burns, fever, adrenocorticotropic hormone therapy, etc.), mostly pre-renal factors, ratio decreased seen too little protein intake, severe liver and kidney dysfunction.
Inflammation of renal fibrosis generally less pathological damage, only mild blood circulation disorders, and injuries limited range, no glomerular and renal interstitial fibrosis, and no change in renal function. But if in the inflammatory response of the disease has not been effectively controlled, then will enter the growth of renal fibrosis, forming period, with a vivid metaphor for the human skin after the process is the formation of scar impaired renal fibrosis, The difference is that the non-proliferation of skin scarring damage, but also damage the kidneys are different ranges have local * early start to spread.
Impaired renal function induced renal cells under inflammatory stimuli role of virulence factors, cytokines, growth factors, occur gradually transformed phenotype, but also to stimulate the kidney fibroblasts into myofibroblasts, synthesis of a series of cellular secretion extracellular matrix, extracellular matrix synthesis increased, their degradation and synthesis homeostasis mechanisms are disrupted, the ultimate cause of a lot of extracellular matrix deposition, and gradually replace healthy kidney units, resulting in glomerular sclerosis continues, tubular - interstitial fibrosis, renal vascular fibrosis. After this time the majority of organizations have kidney fibrosis, the original kidney function were also damaged, the symptoms began to appear complications, serum creatinine, blood urea nitrogen rises; renal filtration rate decreased and so on.

Serum creatinine and blood urea nitrogen levels generally reflect the status of renal function in patients with renal failure, the higher their level, the more serious injury of renal function, serum creatinine more serious damage, the higher the level of urea nitrogen, therefore, active treatment Early kidney disease, lower serum creatinine and blood urea nitrogen, cut the vicious cycle of deterioration of the chain, delaying the development of renal fibrosis.