Speaking of renal failure may be a lot of people will be very afraid, because
we live in the surrounding some families may have lost their lives because of
kidney failure, so we for such diseases are very panic, which should encourage
more people to know more about basic knowledge of renal disease, let's look at
what a reason renal disease caused by?
Cause of renal failure in patients with acute tubular necrosis varied, can be
summarized into two categories:
A renal toxicity to the kidney toxic substances, such as sulfa drugs, carbon
tetrachloride, mercury agents, bismuth, dichloro-sulfamethoxazole
(dichlorphenamide); polymyxin antibiotics, vancomycin, kanamycin Su, gentamicin,
neomycin Pioneer Ⅰ, cephalosporin Ⅱ, neomycin, amphotericin B, and the iodine
contrast agent, methoxy halothane anesthetics; biological toxins such as snake
venom, bee venom, fish, mushroom, cantharidin (Cantharidin), can cause acute
tubular necrosis, under certain conditions.
Second, severe renal ischemia and renal ischemia such as severe trauma,
extensive burns, major surgery, massive blood loss, obstetric hemorrhage, severe
infections, sepsis, dehydration and electrolyte imbalance, particularly with
shock who are easily lead to acute tubular necrosis.
In addition, intravascular hemolysis (eg blackwater fever, primaquine-induced
hemolysis, bean disease, ABO blood transfusion, the oxidation of arsenic
poisoning) released from hemoglobin, as well as muscle mass trauma (such as
crush injuries, muscle inflammation) when myoglobin, by renal excretion, renal
tubular damage may cause acute tubular necrosis. Hereditary nephropathy: as
polycystic kidney disease, Alport syndrome.
Specific pathogenesis of acute tubular necrosis, is not yet fully understood.
It is related to the occurrence of the following:
① extremely reduced glomerular filtration rate (often in 5ml / min or less,
most only 1-2ml / min) generation mechanism may be due to various causes tubular
preceding ischemia or intoxication, renal tubular epithelial cell injury occurs
so that the proximal tubule reabsorption of sodium reduction, so that the
original urine sodium, increase the amount of water. When it flows through the
distal convoluted tubule macula densa, juxtaglomerular stimulation
(juxtaglomerularapparatus) release of renin, angiotensin Ⅱ so that increased
activity in the kidney, causing contraction of glomerular small artery spasm,
leading to glomerular especially in the outer cortical blood flow decreased
glomerular, filtration rate is extremely reduced.
② tubule lumen obstruction after injured necrosis, loss of renal tubular
epithelial cells and inflammatory exudate, blood (muscle) red protein, forming
clumps and tube, blocking the lumen, so that the original dirty urine is
blocked, thus oliguria; on the other hand lumen urine swelling, will increase
pressure on the kidney, the glomerular filtration rate decline further.
③ renal tubular wall rupture, the original urine spill. After the injured
tubules, wall rupture, the original urine tube to tube overflow, thus oliguria;
while renal interstitial edema caused by increased pressure on the kidney, the
glomerular filtration rate.
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