The hazards of Chronic Nephropathy

Patients with chronic kidney disease is a variety of symptoms, the symptoms of edema and hypertension are more common, however, the most obvious is the most harmful is proteinuria. Such symptoms with the naked eye can not see, and this symptom treatment is more troublesome.
Proteinuria, although not particularly obvious, but if it is chronic kidney disease must check whether the emergence of such symptoms, and should make the treatment measures in a timely manner. Chronic kidney disease proteinuria is not only a sign of kidney damage, a large number of proteins by tubular excretion will trigger the inflammation and fibrosis of the renal tubular epithelial cells, thus accelerating the development of chronic kidney disease. Recent studies have confirmed that a large number of urinary protein to promote the progress of chronic kidney disease to one of the major risk factor for end-stage renal failure, and should therefore be used as the important goal of the treatment of chronic kidney disease. Glomerular mesangial toxicity of the urine protein: proteinuria nephropathy model, low-density lipoprotein (LDL) and very low density lipoprotein (VLDL) apolipoprotein B and apolipoprotein A deposition gathered eventually be leading to glomerular sclerosis. Urinary protein toxic effects on proximal tubule cells: proteinuria, enter the amount of protein within the renal tubular epithelial cells to increase, so that the increase of lysosomal activity, suggesting that the protein caused lysosomal spilled into the small tube cytoplasm, followed by cell damagecan stimulate inflammation and scar formation.
Weifang, Shandong Red Sun nephropathy hospital experts pointed out that the protein in the urine of chronic kidney disease often make friends of patients are not very understanding, but also often ignore the dangers of tubule cell biological changes caused by the urine protein is a very serious and urine protein many kidney disease there is excessive proliferation of cells, represents a non-adaptive responses, leading to renal failure. More and more evidence to show that the protein can be directly conditioning tubule cell function, to change its growth characteristics of cytokines and matrix proteins phenotypic expression, the basal side of the tubule can lead to release of PDGF, FN and MCP-1 induced fibrosis. The urine protein to cause tubulointerstitial hypoxia aggravated: proteinuria re-absorption of a large number of proteins in each digest extra energy can cause tubular cell hypoxia, resulting in the tubule cell injury.