Immediately after the previous article of proteinuria 1 +, urine protein often suggests that there may be nephritis. But the urine test is also the existence of false positives, that is, perhaps by the vacation, specimens taken by the irregularities of the composition of the original urine and no protein, but the results are positive. So, what are the factors that make up urine protein 3+? Next Tan Feng doctor continue to give you an introduction: urine protein 3 + factors mainly because of infection and other pathological damage caused by the patient damaged kidney part of the microcirculation obstacles, promote the renal arrangement ischemia, hypoxia, once the damage to the renal vascular endothelial cells. Damaged renal capillary endothelial cell function changes, the dynamic balance of function is disturbed, inviting the blood circulation of inflammatory cells infiltration, that is, constitute an inflammatory response, synchronized start renal fibrosis, glomerular basement membrane damage, its filtration aperture increases or atresia, basement membrane cracking, charge barrier is damaged, the renal permeability increased, can not be useful to block protein leakage, and then clinically constitute urinary protein! So what are the hazards of proteinuria 3+? 1, caused by the tubular cell biological shaking, the emergence of urinary protein in many kidney disease there is cell overgrowth, representing a non-adaptive response, resulting in renal failure. Protein can directly regulate tubular cell function, change its growth characteristics and its cytokine and matrix protein phenotype expression, can lead to tubular basolateral release of PDGF, FN and MCP-1, inducing fibrosis. 2.Tethering membrane toxicity, in the renal failure model, it can be observed that serum proteins accumulate in the glomerular tethering membrane, and the collection of those macromolecules in the tethering membrane area can lead to the damage of tethering membrane cells, hyperplasia of the composition of the tethering membrane matrix increases, and then the onset of glomerulosclerosis. In the model of urinary protein nephropathy, the accumulation of apolipoprotein B and apolipoprotein A in the glomeruli with low-density lipoprotein and very low-density lipoprotein can also lead to glomerulosclerosis. 3, the glomerular filtration membrane is damaged, resulting in increased permeability of the glomerular filtration membrane permeability means that the initiation of renal fibrosis, if not timely treatment, the further extension of the disease, the renal intrinsic cell phenotype will be transformed to generate not easily degraded collagen fibrous proteins, accumulating in the kidneys, gradually replacing the healthy renal units, and ultimately will be carried out into the final stage of renal failure – uremia. 4, resulting in tubular interstitial hypoxia increased, urinary protein reabsorption of each digestive protein rated energy, can constitute tubular cell hypoxia, resulting in tubular cell damage. Warmly suggests: proteinuria 3 + is the kidney “hole” began to slowly become larger, and is the loophole began to increase when. If you can choose the right method to repair the “hole”, the proteinuria will gradually reduce, if you take the method is not appropriate, it is very likely to make the condition more serious, so that the uremia signs and uremia signs. I believe you should have some understanding. So, the proteinuria must trigger our attention, not easy to be taken seriously.