Chronic renal failure can cause kidney structure and function of the changes?

Chronic renal failure occurred in the course of development and there can be a series of kidney structure and function of compensatory responses Due to enable the body to reduce the number of renal units arising in different changes to maintain body balance. The structure and function of these compensatory responses include the following: ① units residual renal glomerular filtration rate increase to compensate for the loss of renal function units, in the excretion of metabolic waste, but because of the residual renal units heavier load, has further accelerated the glomerular damage, such as by causing kidney small ball mast; ② compensatory glomerular hypertrophy, although in complete renal units without adverse reaction, but can also enhance the renal function, but in glomerular disease can cause secondary glomerular filtration rate decline accelerated glomerular the hardening; ③ glomerulosclerosis and interstitial infiltration of inflammatory cells, can be swallowed, removed from glomerular and tubular damage harmful substances, but it may also be the release of growth factors and inflammatory mediators, the deposition of collagen and stimulate mesangial matrix increase, leading to kidney small ball sclerosis and tubulointerstitial fibrosis appeared ④ residual renal sodium excretion increased units, can prevent expansion of extracellular fluid and have high blood pressure, but reducing sodium intake can be caused by low capacity reaction; ⑤ tubular secretion increased ammonia, acid poisoning can be reduced although the selection, but it accelerated tubulointerstitial injury; ⑥ urinary protein excretion in patients with edema could lead to an increase, hypoproteinemia, and accelerate renal glomerular damage; ⑦ secondary hyperparathyroidism, the body increases the excretion of phosphorus, reducing phosphorus retention, but its consequences is a cause of uremic osteodystrophy and other organ function of disorder and imbalance. Evidently, chronic renal failure occurred during a series of kidney structure and function of compensatory response, though correct renal units can be part of a series leading to the loss of pathophysiological changes, but if we do not artificially their positive control, have the potential to bring about adverse effects of the body, could eventually lead glomerulosclerosis and tubulointerstitial damage. The glomerular sclerosis is a variety of reasons renal injury induced renal function units can reduce residual pressure within the glomeruli significantly increasing glomerular capillary pressure increase caused glomerular endothelial cell injury, micro-artery Tumor formation and platelet aggregation and thrombosis leading to glomeruli, and the region as mesangial macromolecular material gathered partial release of growth factors and the impact of mesangial cells, mesangial matrix expansion, can cause residual renal small ball compensatory hypertrophy, excessive compensation that is the ultimate end glomerulosclerosis. Renal tubular injury was due to the residual renal tubular units significantly heavier load, resulting tubular high metabolism, tubular epithelial cells in the enhancement of the activity of renal tubular damage caused. Chronic renal failure pathophysiological process is extremely complex, but is generally believed that the following factors in chronic renal failure in the structure and function of the kidney plays an important role in change: ① glomerular capillary blood pressure increased; ② systemic hypertension; ③ glomerular coagulation; ④ increased serum lipid levels; ⑤ kidney local cytokine activity and angiotensin system changes; ⑥ tubular high metabolism. Therefore, the clinical response to these factors can be used to strictly control blood pressure levels, lower pressure within the glomeruli, anticoagulant therapy, kidney partial control the level of angiotensin II, hypolipidemic treatment and low-protein diet, and so delaying chronic renal failure progress.