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The pathogenesis of chronic renal failure in the elderly

Dec 31, 2016
Chronic renal failure: the mechanism of progressive deterioration slow renal failure mechanism is complex, has not yet fully understood, has the following main doctrine:
1. The woods nephron theory and revisionist-reformist imbalances theory Renal parenchyma disease causes quite a number of renal units, the rest of the woods to compensatory renal unit, have to work more, in order to maintain the body's normal needs.Thus, each nephron compensatory hypertrophy, in order to enhance the glomerular filtration function and renal tubular to deal with the function of the filtrate.But such as the destruction of the renal parenchyma disease continue, woods nephron less and less, finally arrived even our best, can't meet the minimum requirements of the human body metabolism, has kidney failure, this is the woods nephron doctrine.When failure occurs, there will be a series of pathological phenomenon.To rectify it, and the body will be adjusted accordingly (correct), but in the process of adjustment, but inevitably pay a price, and the new imbalance occurred, new damage to human body.For example: when the woods nephron decreased, the rest of the each nephron compensatory amount of phosphorus discharge increased, from the kidney, the discharge amount of phosphorus can still be normal, so the blood phosphorus is normal.But when later woods renal units to cannot be compensated, blood phosphorus is increased.The human body to rectify the phosphorus retention, hyperparathyroidism, in order to promote kidney phosphorus, hyperphosphatemia is improved at this moment, but hyperparathyroidism caused the other symptoms, such as due to dissolve bone extensive fibrous osteitis and the toxic effect of nervous system, etc., a new damage to the human body.This is revisionist-reformist imbalance theory, it is the development of the theory of woods renal units and supplement.
2. High glomerular filtration theory When renal unit damage to a certain number, the rest of the each nephron metabolic waste discharge load increase, thus high happen in compensatory glomerular capillary perfusion, high pressure and high filtration.And the "three highs" within the glomerulus can cause: (1) glomerular epithelial cell foot process fusion, mesangial cells and matrix hyperplasia, glomerular hypertrophy, and cirrhosis;(2) the glomerular endothelial cell damage, induce platelet aggregation, lead to thrombosis, glomerular damage and promote hardening;(3) increased glomerular permeability, increase the proteinuria and renal tubular interstitial injury.The above process is ongoing, form vicious circle, make continuously worsening renal function.This vicious cycle is the common way to all chronic kidney disease development to uremia, and the destruction of the renal parenchyma disease continue are two different things.
3. The renal tubular high metabolic theory Slow renal failure, the woods of nephron compensatory high metabolic state, renal tubules is increased oxygen consumption, increase oxygen free radicals, and renal tubule cells to produce ammonium increased significantly, can cause damage to the renal tubules and interstitial inflammation and fibrosis, and loss of renal unit function.Has been clear, the progress of chronic renal failure and renal tubular closely related to the severity of the damage.
4. Some scholars think that other slow progressive deterioration mechanism of renal failure is associated with the following: (1) under the condition of "three highs" within the glomerulus, increased levels of angiotensin Ⅱ was found in the kidney tissues, such as growth factors increase growth factor expression, lead to increased extracellular matrix, and glomerular sclerosis;(2) from too much protein in the glomerular filtration, will cause high glomerular filtration, and proximal convoluted tubule cells by pinocytosis after protein absorption, can cause renal tubular and interstitial damage, leading to renal unit function is lost;(3) lipid metabolic disorders, low density lipoprotein can stimulate mesangial cell hyperplasia, and glomerular sclerosis, deterioration of renal function.

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