The pathogenesis of renal failure

The pathogenesis of the disease complex, is not yet fully understood.
1. Health nephron unit theory
Various causes of renal parenchymal disease, leading to most of the kidney unit damage. Residual small part of the normal damage to the function of the normal kidney unit, due to the normal needs of the body to compensate for the doubled work. Resulting in "health" of renal units in the compensatory hypertrophy, glomerular filtration function and renal tubular processing filtrate function enhancement, and ultimately lead to glomerular sclerosis and loss of function. Finally, "health" nephron gradually reduced, gradually diminished renal function.

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2. uremic toxins doctrine
Uremic toxins, may be renal failure accumulated in the body of a variety of substances, including PTH, phosphorus, urea, creatinine, guanidine, phenols and indole and so on.
These substances have the following characteristics:
① body concentration content higher than normal.
② high concentration and specific symptoms of uremia.
③ can be carried out chemical identification and quantitative determination.
④ substance concentration and uremic patients with similar concentrations of body fluids, the emergence of similar toxic effects.

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3. The theory of imbalance
Renal insufficiency when the body showed a series of pathological symptoms, the body for the corresponding adjustments to correct, but the compensatory change but led to a new imbalance, that imbalance, and thus produce a series of clinical symptoms. Such as phosphorus metabolism.

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4. Glomerular hypertension and compensatory hypertrophy theory
Health neonatal unit of the small arterial resistance decreased, and the ball out of small arterial resistance increased. Leading to high pressure in the glomeruli, high perfusion and high filtration. Glomerular hypertension to thick arterial wall thickening and capillary wall tension increased, causing ischemia and endothelial cell damage, mesangial cells and matrix hyperplasia, to promote the residual glomerular compensatory hypertrophy, glomerular sclerosis, renal function Further deteriorated.
5. Tubular hyperglycemia
Residual renal units of the renal tubules, especially proximal renal tubules, the metabolism of hyperthyroidism, oxygen free radicals increased, cell damage, so that tubulointerstitial lesions continued, renal unit function loss.

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