2016年8月8日星期一

Chronic renal failure, renal what changes

The development and progression of chronic renal failure can occur compensatory response to a series of kidney structure and function, so that the body adapt to the body due to the reduced number of units of renal function caused by various changes, maintain the balance of the body. These compensatory response of the structure and function mainly includes the following aspects:

①, residual nephron glomerular filtration rate increases, action to compensate for the loss of nephron function, the body excrete metabolic waste, but due to the load of residual renal units increase, further accelerated glomerular damage, such as cause glomerular hypertrophy;

②, glomerular compensatory hypertrophy, although no adverse reactions in intact nephrons, and can enhance renal function, but in glomerular diseases can cause secondary glomerular filtration rate decline, renal acceleration ball hardened;

③, glomerular and interstitial inflammatory cell infiltration, it can be swallowed, causing glomerular remove harmful substances tubular damage, but can also release growth factors and inflammatory mediators, stimulate collagen deposition and mesangial matrix increase, leading to kidney glomerulosclerosis and interstitial fibrosis occurs between the tubular;

④, residual renal sodium excretion unit can prevent high blood pressure and extracellular fluid expansion generated, but reducing sodium intake can cause low-volume reaction;

⑤, tubular secretion of ammonia increased, although you can reduce the production of acid poisoning, but accelerated tubulointerstitial damage;

⑥, it can lead to increased urinary protein excretion in patients with edema, hypoalbuminemia, and accelerate the tubular glomerular damage;

⑦, secondary hyperparathyroidism, increased so that the body of phosphorus excretion, reducing phosphorus retention, but its consequences are caused disorder and imbalance uremic bone disease and other organ function. Thus, compensatory response to chronic renal failure occurred during a series of kidney structure and function, although partially corrected nephron loss resulting from a series of pathophysiological changes, but if you do not artificially be a positive control, They are likely to have adverse effects to the body, can eventually lead to glomerulosclerosis and tubulointerstitial damage.

Glomerular sclerosis is due to various causes of kidney damage kidney function unit can decrease significantly increased residual glomerular pressure, glomerular capillary pressure increases, causing glomerular endothelial cell injury, arterioles tumor formation and platelet aggregation caused by thrombosis in glomeruli, the other due to the aggregation and local mesangial area macromolecules release of growth factors on cell proliferation, mesangial matrix expansion, can cause residual glomerular compensatory hypertrophy, excessive compensation is the final outcome of glomerulosclerosis.

Renal tubular damage is due to residual renal tubular unit load Ming significantly increased, leading to high metabolic tubular and tubular epithelial cell activity enhancement caused by renal tubular damage.

Pathophysiology of chronic renal failure is extremely complicated, but it is generally believed that changes in the following factors in chronic renal failure, renal structure and function play an important role:

①, glomerular capillary blood pressure;

②, systemic hypertension;

③, glomerular coagulation;

④, serum lipid levels increased;

⑤, kidney and local cytokine changes angiotensin system activity;

⑥, tubular high metabolism.

Therefore, clinical response to these factors can be strict control of blood pressure levels and lower glomerular pressure, anticoagulation therapy, local control of renal angiotensin Ⅱ level, lipid-lowering therapy and low-protein diet to slow chronic renal failure Progress.

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