Oliguric renal failure in what stage of performance characteristics

Oliguric acute renal failure generally can be divided into the pathogenesis of oliguria , polyuria and recovery stages.
Oliguria : This significant reduction of urinary plate , and the accumulation of metabolites in vivo . Water, electrolyte and acid-base balance disorders . It is the most dangerous phase of the course .
( 1 ) change little or no urine and urine components : acute renal failure scorpion appears little or no urine mechanism with reduced GFR, original urine leakage from the back room of tubular necrosis and tubular obstruction and other qualitative factors. When the original urine by renal tubular damage , due to the dysfunction of renal tubular epithelial reabsorption of water and sodium , so the low specific gravity , urine osmolality less than 350mOsm / L, urine sodium containing t higher than 40mmol (40mEq) 1? Chang up to 80-IOOmmol (80-100mEq / L). As the glomerular filtration dysfunction and renal tubular epithelial necrosis, urine contains protein . Red, white and various casts. These changes and functional changes in acute renal failure urine when there are significant differences .
( 2 ) water intoxication : Because the kidneys severely reduced urine output , to strengthen the body so that the increased catabolism of raw water , and inputs such as excessive solution to turn grapes Chu reasons , can cause body water bet to stay . When the water left over sodium Han Yi left , can cause dilution hyponatremia , water can be transferred to the cells and cause cell swelling . Patients may be complicated by severe pulmonary edema, cerebral edema and cardiac dysfunction . So the end of acute renal failure interest , should be closely observed and recorded the person water t, and strictly control the speed and rehydration supplement tuck t.
( 3 ) hyperkalemia : This is Tim acute renal failure in patients with the most dangerous changes. ① cause hyperkalemia is a significant reduction in urinary dish , urinary potassium excretion decreased ; ② tissue injury , cellular catabolism , hypoxia, acidosis Inso potassium can promote the transfer of cells from the outside inward ; ③ banked blood potassium intake of food or a large surplus of people with high concentrations of potassium shaft and so on. Hyperkalemia can cause cardiac excitability decrease induced arrhythmias , and even lead to cardiac arrest and endanger the patient's life .
( 4 ) metabolic acidosis : renal excretion of acid is mainly due to the dysfunction caused by child protection , with progressive and difficult to correct characteristics. Acidosis inhibits the cardiovascular system and central nervous system , and can promote the occurrence of hyperkalemia .
( 5 ) azotemia : protein metabolism because the body can not adequately excreted by the kidneys , and often enhanced protein catabolism , it contains blood urea , creatinine and other non-protein nitrogenous substances t can be greatly increased, called nitrogen quality hyperlipidemia (emternia). Usually in the first few days after oliguria . Have significantly increased blood non-protein nitrogen . Infection , poisoning , tissue trauma so severe blood non-protein nitrogen levels will be further increased.
Sustainable oliguria days to weeks . An average of 7-12d. Oliguria continued longer the worse the prognosis . If the patient can safely spend oliguria . And when the body has renal tubular epithelial cell regeneration. You can enter polyuria .