The risk of proteinuria in nephrotic syndrome

The risk of proteinuria in nephrotic syndrome

What are the dangers of proteinuria in nephrotic syndrome patients?
In patients with nephrotic syndrome, one is a symptom of the most a large number of urine protein, urine protein is not only due to the loss of a large number of protein, and urinary protein in glomerular and renal tubular will cause damage, resulting in renal fibrosis. Studies have shown that the occurrence of urinary protein is the first independent risk factor for uremia. The biggest hazard of urine protein is that it can destroy the kidneys and cause uremia. So, what are the specific hazards of urine protein?
First of all, the urinary protein toxicity of the membrane
In renal failure model, can be observed in the accumulation of serum protein in mesangium, aggregation of these macromolecules in the mesangial area can cause mesangial cell damage, proliferation of the mesangial matrix increased synthesis, resulting in glomerulosclerosis. In the nephrotic model, urinary protein contains low density lipoprotein (LDL) and very low density lipoprotein (VLDL) apolipoprotein B and apolipoprotein A deposits, and these aggregates eventually lead to glomerulosclerosis.
Secondly, the toxic effects of urinary protein on proximal convoluted tubule cells
When the occurrence of urinary protein, protein in renal tubular epithelial cells into lysosomes increased, the activity increased, suggesting that the lysosomal protein spilled into the tubular cytoplasm, subsequent cell injury can stimulate inflammation and scar formation.
Thirdly, the biological changes of tubular cells induced by urinary protein
In general, many renal diseases with proteinuria appear to have an overgrowth of cells, which represents a non adaptive response that can lead to kidney failure. More and more evidence that the protein can be directly regulating tubular cell function, change the growth characteristics and phenotypic expression of cytokines and matrix protein, can lead to the release of PDGF and FN tubular basement side and MCP-1 induced fibrosis.
Finally, proteinuria results in increased tubulointerstitial hypoxia
Urinary protein reabsorption, digestion of large amounts of protein requires extra energy, can cause tubular cells hypoxia, resulting in tubular cell damage.
Comprehensive content of the above shows that the absence of urinary protein is very unfavorable for patients with nephrotic syndrome, so attention should be paid to timely treatment. If you have any further questions, please contact our online doctor or leave a message for us. We will reply to you as soon as possible.
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