The general cause of proteinuria is damage to kidney function, which leads to problems with filtration and absorption. If not treated in time, kidney function will continue to be damaged. In more severe cases, it can lead to kidney necrosis, which is life-threatening. The hazards of proteinuria are mainly manifested in the following aspects: (1) Mesangial toxicity of proteinuria can be observed as the accumulation of serum proteins in the glomerular mesangium. The accumulation of these macromolecules in the mesangium can cause mesangial cell damage, proliferation, and increased synthesis of mesangial matrix, thereby producing glomerular sclerosis. In the proteinuric nephropathy model, apolipoprotein B and apolipoprotein A deposits of low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) are present in the glomeruli and these aggregations can eventually lead to glomerular sclerosis. (2) The toxic effect of proteinuria on proximal tubular cells increases the amount of protein entering the tubular epithelial cells, which increases the activity of lysosomes, suggesting that protein causes lysosomes to overflow into the tubular cytoplasm. The subsequent cell damage can stimulate inflammation and scar formation. (3) The biological changes in tubular cells caused by proteinuria represent a maladaptive response, leading to renal failure. There is increasing evidence that proteins can directly regulate tubular cell function, alter their growth characteristics and their phenotypic expression of cytokines and matrix proteins, leading to the release of PDGF, FN, and MCP-1 from the basal side of the tubules, inducing a fibrotic process. (4) Proteinuria aggravates tubular interstitial hypoxia, which can cause tubular cell hypoxia and thus tubular cell damage. |
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