Acute renal failure Why is there non-oliguria performance? What is the mechanism?

Non-oliguria acute tubular necrosis is not oliguric or non-performance of urine acute tubular necrosis, The non-oliguria pathogenic factors and oliguria different, the former is due to renal aminoglycoside antibiotics and toxic substances caused by contrast medium, and oliguria more from surgery, renal ischemia lead. Non-oliguria, urine testing indicators of changes in less light. Such was Zhang urine, urinary sodium content less Pai sodium scores lower, less than one percent, serum creatinine increased lesser extent / renal function faster, non-oliguria the merger, those of less urine - less mortality is low, less need dialysis. But the mortality rate still 26 percent, individual treatment of serious patients need dialysis. Non-oliguria in recent years the incidence of acute renal failure increased year by year, up 70% -80%. Apart from the increased awareness of this disease, in recent years due to increased use of aminoglycoside antibiotics, and drug-induced acute tubular necrosis and more non-oliguria. Moreover, acute renal failure early rational use of diuretics, such as mannitol and dopamine increased urine of renal blood flow and scour role, and are often non-performance of oliguria. Now that non-oliguria acute tubular necrosis of the pathogenesis of mainly due to the following three points: ① injury in the kidney unit is not identity. In addition to renal units exist identity, the liquid dynamic renal units changes also different. Non-oliguric renal units of kinetic changes in the liquid between the larger differences, some renal perfusion units renal blood volume is not reduced, no significant vasoconstriction, and vascular resistance is not high and the other body part of the renal units in renal perfusion less significant vasoconstriction, and vascular resistance increased renal ② in the same flat, glomerular and tubular damage were also inconsistent. The severity of renal damage units do not - and the extent of glomerular damage also different. Because of glomerular damage, it decreased glomerular filtration rate, blood urea nitrogen and serum creatinine were higher. But in certain units because of renal tubular damage to light, sodium, water transit dysfunction light, it excretion of sodium and water excretion scores scores are higher, resulting in urine output is not reduced; ③ Coligorsky set forth in sublethal acute renal failure renal tubular obstruction mechanism assumptions. The only group in the early cellular damage - damage to the basement membrane adhesion, there will be the proximal tubular epithelial cells exfoliated from the substrate, seen in the tubular cavity. Yet there cells - cells interaction, within the lumen and gathered into groups and / or loss of exfoliated epithelial cells and cell adhesion, and obstruction lumen. These cells can be exfoliated luminal fluid and urine out there. Morphological examination showed continuity small cell wall damage, there fissures, and function tests can confirm a return to leakage phenomenon. This non-clinical stage and oliguria with acute renal failure.