Acute renal failure.

acute renal failure is a variety of causes caused by a sharp decline in renal function of the kidneys, resulting in serious disorders of the body environment clinical syndrome. Clinically, it is mainly manifested as nitrogenemia, high potassiumemia and metabolic acidosis, and is often accompanied by less or no urine.

1, Causes and Classification of Acute Renal Failure

According to the cause of the disease, acute renal failure can be divided into three major categories: pre-renal, renal and post-renal.

(i) Pre-renal acute renal failure

Pre-renal acute renal failure is caused by a sharp decrease in blood flow to the kidneys, commonly found in the early stages of shock. At this time, the effective circulation of blood volume and blood pressure reduction in addition to directly lead to a decrease in renal blood flow, but also through the cross-sensory-adrenal myelin system and the epinephrine-angiotensin system to make the kidney arteries strongly contract, thereby further reducing the blood flow of the kidneys and effective filtration pressure.

GFR has been significantly reduced. At the same time, secondary aldehyde ketones and ADH secretion increased, but also to enhance the re-absorption of sodium and water by distant small tubes and collection tubes, so that the amount of urine significantly reduced, the content of sodium urine is less than 20mmol (mEq)/L, the proportion of urine is higher. The sharp reduction of GFR can also cause high potassiumemia and acid-base balance disorders.

Because of pre-renal acute renal failure fashion no renal substance of the organ damage, so when blood volume, blood pressure and heart output due to timely treatment and return to normal, kidney urinary function also immediately returned to normal. Therefore, this is generally considered to be functional acute renal failure, but if renal isoemia persists for too long, it can cause renal damage, which can lead to renal acute renal failure.

(ii) Acute renal failure

caused by renal lesions is called renal acute renal failure. For example, acute globular nephritis and lupus nephritis (see systemic lupus erythematosus), due to inflammatory or immune damage, can cause a large number of renal globular dysfunction, which can cause acute renal failure. Double-sided renal artery embolism can also cause acute renal failure. In addition, acute pyelonephritis, eclampsia, nodding polyarthritis, etc. can also cause acute renal failure.

, however, it is more common clinically to have acute renal failure caused by acute renal tube necrosis caused by renal ischemics and renal poisons. There are two types of causes of acute renal tube necrosis.

1. Renal isoemia is found in shock cases caused by various causes and is not rescued in a timely and effective manner. At this point, severe and persistent blood pressure drops and strong contractions of the nephrotic arteries can significantly and continuously reduce blood flow to the kidneys. As a result, ischemic damage can occur in the kidney tubes and even necrosis.

, even if blood volume is corrected and blood pressure returns to normal, kidney urinary function cannot be restored quickly. The patient's urine contains < a href"" > protein red, white blood cells and various tube types. The concentration of sodium urine can generally be raised to 40 to 70 mmol (40 to 70 mEq)/L or higher, indicating that the renal tube has been damaged and the function of sodium protection has been reduced.

2. Renal toxic heavy metals (mercury, arsenic, palladium, lead), antibiotics (methamphetamine, neomycin, polymycin, gydamycin, avant-gardemycin, etc.), sulfonamide, certain < A href"">"< organic compounds (carbon tetrachloride, chloroform, methanol, phenol, toluene, etc.), insecticidal drugs, toads. Some blood vessels and kidney gloom agents, snake venom, myoglobin, etc. can directly damage the kidney tube, and even cause necrosis of the epithal cells of the renal tube. At this time, if the blood flow of the kidneys is insufficient, it will aggravate the damage of the kidney tube.

in many pathological conditions, renal isoemia and renal poisons often occur simultaneously or one after another. For example, when the role of renal poisons, local vascular spasms in the kidneys can lead to renal isoemia; It is generally believed that kidney isoemia, coupled with the role of renal poisons, is most likely to cause acute renal failure.

renal failure caused by acute renal tube necrosis. Clinically, according to the need for less urine can be divided into less urine type and non-less urine type two categories. Less urine type is more common, patients empty appear less urine (adult 24 hours of urine less than 400 ml) or even no urine (24 hours of urine less than 100 ml). The amount of urine in patients with non-low urine type does not decrease, and can even increase, but nitrogenemia worsens day by day, this type accounts for about 20%.

(iii) post-renal acute renal failure

urinary tract obstruction from the kidney to any part of the urethra mouth, may cause post-renal acute renal failure. Obstruction above the bladder is mostly caused by stones.

However, due to the powerful compensation reserve of the kidneys, post-renal acute renal failure is caused only when stones obstruct both sides of the urinary tract at the same time or the kidneys on one side are incapaction and the urinary tract on the other side is blocked. Obstruction of the bladder and urethra can be caused by bladder dysfunction (such as chronic urinary retention caused by spinal cord rickets, diabetic prosthetic spinal cord pyridosis, etc.) or by hypertrophic prostate and prostate cancer.

in the early stages of post-renal acute renal failure did not have renal-essential organomorphic damage. Remove obstructions in a timely manner. It can restore the urinary function of the kidneys quickly. Therefore, such patients should be clearly diagnosed at an early age and treated appropriately.

II, pathogenesis of acute renal failure

The pathogenesis of acute renal failure currently refers to the pathogenesis of renal failure caused by acute renal necrosis. In the exploration of the pathogenesis of acute renal failure, in addition to clinical observation, autopsy or livetissue examination, animal models of acute renal failure caused by various methods are often used for analysis and research.

For example, animals can be injected with mercury, uranyl nitrate, lead compounds, etc. caused by toxic acute renal failure, or by narrowing the adrenal arteries, the adrenal arteries continue to inject dethyroidism, causing hemorrhagic shock and other methods to cause ischemia renal failure, but also intramuscular injection of glycerin caused by myoglobin and lead to acute renal failure.

In the above animal model, because the factors causing kidney damage are more complex, no experimental model can fully explain the pathogenesis of acute renal failure and can only suggest the role of the relevant factors from one aspect.

It should therefore be noted that the pathogenesis of acute renal failure described below is an overview of the results obtained from different animal experimental models, and that these experimental data may not fully clarify the pathogenesis of acute renal failure as seen clinically.

(i) The original urine back into the interstitial

the application of micro puncture method to inject 14C-chrysanthemum powder directly into the kidney cavity of the kidneys on the side of the rat damaged by ischemia or injection of uranium nitrate oxygen in the kidney arteries, a large amount of radioactive chrysanthemum powder can be found in the urine generated by the kidneys on the other side. This confirms that the renal tube epithal cells of the damaged kidneys are highly permeable, allowing chrysanthemum powder to enter the whole body's blood circulation through a leakback and be excreted by the side kidneys.

So it is believed that persistent renal ischemic or renal toxicity causes necrosis of the epithelirsty of the renal tube and in turn leads to acute renal failure, the primary urine in the tube cavity of the kidney can directly reduce the amount of urine, on the other hand, by forming interrenal edema and compressing the renal tube and hindering the passage of primary urethra, the result is a further reduction of GFR.

recent trials of ischemic and toxic renal failure have found a decrease in urine production before necrosis of epithal cells in the renal tube. Clinically, renal cystic excision is performed on some patients with acute renal failure to reduce interrenal edema and does not improve renal urinary function. Therefore, it is now believed that the primary urine leakage caused by necrosis of the kidney tube is not the primary mechanism of acute renal failure and less urine, but can make less urine aggravate.

(ii) Renal tube blockage

hetero-transfusion, extrusion injury, etc. cause acute renal failure, in the pathological tissue slice can be found necrosis shedding epithelial cell fragments, myoglobin, hemoglobin, etc. formed by the tube blocking renal tube. In animal experiments of acute renal failure, various tube types have also been seen in renal tubes. Therefore, renal tube obstruction may be one of the pathogenesis that causes less urine in acute renal failure.

the renal tube is blocked, the pressure in the tube cavity of the renal tube can be increased and GFR reduced. However, in the experiments of acute renal failure caused by renal ischemics and renal poisons, when micro-perforation was used to determine the pressure in the renal tube near the obstruction, most of the experimental data showed that the pressure in the tube did not increase, or even decrease.

believe this is due to a reduction in GFR due to the contraction of the renal ocular artery through the tube-ball feedback mechanism (tubuloglo-merular feedback mechanism). Therefore, it is difficult to confirm the primary mechanism of less urine when renal tube obstruction causes acute renal failure.

also proved that when GFR returned to normal and raw urine formed sufficiently, the tube type could be washed away and it was not easy to form a renal tube blockage. This also shows that the blockage of the kidney tube is the result of the reduction of GFR. However, after the existing renal tube is blocked, it can contribute to the deterioration of renal failure.

(iii) Renal ococyts filter dysfunction

In the pathogenesis of acute renal failure, renal ococyspheric filtration dysfunction is paid more and more attention. The main factors that cause the dysfunction of renal filtration are the decrease of blood flow of kidneys, the decrease of effective filtration pressure of kidney ococyts and the change of permeability of the membrane of renal ococyts, which are described below.

1. Reduced blood flow to the kidneys using inert gas washout, dye dilution,isotope mark microsphere perfusion and electromagnetic flow When measuring blood flow to the kidneys, it was found that patients with acute renal failure, as well as animals with acute renal failure caused by renal isoemia or renal poisons, had reduced blood flow to the kidneys, and generally reduced by about 45 to 60%.

the most obvious reduction of renal cortological blood flow, i.e. abnormal distribution of blood flow in the kidneys, resulting in serious disorders of renal urinary function. However, the application of diazepam, acetylcholine, prostatin and other treatment of acute renal failure, in the kidney blood flow and renal cortive blood flow increased, can not improve GFR. Therefore, reduced blood flow to the kidneys may not be the main pathogenesis of acute renal failure.

2. The experimental data on effective filtration pressure reduction of renal cystic balls indicate that when renal isoemia and renal toxicity cause acute renal failure, it can sometimes be seen that the content of cerpamine and angiotensin II in the blood increases, which may lead to the contraction of the small arteries of renal cylindrology, so that the effective filtration of renal cylindrology and filtration rate is reduced, among which angiotensin II.

recent experimental data show that when acute renal failure occurs, the content of angiotensin in the outer layer of the renal cortical system increases. Recently, it has also been found that renal tissue nephrine, in the kidney can also form angiotensin II. , and thus cause the ball artery contraction, so that the blood flow of the renal cyst is reduced, effective filtration pressure and filtration rate is reduced.

increased activity of the end-renal renin-angiosin system during acute renal failure may be caused by a tube-ball feedback regulation mechanism.

Experiments show that after renal ischemia and renal toxicity cause dysfunction of the renal tube, the re-absorption function of the near-curvy tube on sodium is reduced, the concentration of sodium in the far-curvy tube increases, so that the dense spot is stimulated by the sodium load and causes the renal secretion to increase, the formation of endovascular tension II.

the role of the end-renal nephrine-angiolycerline system in the pathogenesis of acute renal failure is not fully confirmed. For example, experimental data show that chronic salt-loaded renal renin depletion does not prevent the occurrence of certain experimental acute renal failure, when the kidney tissue contains high concentrations of renin (aggressive renal vascular hypertension), usually not accompanied by acute renal failure. The issue therefore needs to be further explored.

3. When the change experiment of renal cytosphere filter membrane permeability proved that when the dog's side of the nephrical artery continued to drip high concentrations of epinephrine caused acute renal failure, a scanning electron can observe a significant morphological change in the epithelial cells of the organ layer of the cylindrical cyst - epithelial cells fuse with each other and normal filter gaps disappear.

In this time, if the experimental dog input salt water to increase the blood flow of the kidneys, and can not increase the amount of urine, so it is believed that the above morphological changes in the kidney phospherics, may be the cause of the kidney ococyte filter dysfunction." In other animal models, however, renal balls generally do not show this morphological change.

Also found in animal models of isoemia and toxic renal failure are swelling of renal cytovascular endothritis cells and renal cystic epithellal cells, which are thought to reduce blood flow to the cytosis and alter the permeability of the membrane. However, these changes are generally believed to occur only in the initial stages of acute renal failure, as rather than as a major mechanism for GFR reduction in acute renal failure.

, it can be seen that the pathogenesis of renal failure caused by acute renal tube necrosis is complex. Among them, renal ball filtering dysfunction may play a more important role. The mechanism that causes renal cystic filtration dysfunction, in addition to renal cystic lesions and kidney blood flow reduction directly causes the reduction of renal cystic blood flow, can also be damaged by the renal tube, through the tube-ball feedback regulation mechanism, causing the activity of the renal nephrine-angiostrain system to increase.

cause the ball artery to contract, so that the kidney cytofiltration and filter rate continues to decrease. Primary urine leakage caused by necrosis of epithelocytes in the renal tube and obstruction of the renal tube may also play a role in the onset of acute renal failure.