Best Hospital for Kidney Disease

Email US:763363721wxn@gmail.com   Call Us:0086-15176446195

Pathology of renal insufficiency

Dec 25, 2016
To thoroughly treat renal insufficiency, we should first understand its pathogenesis pathology, fundamentally eliminate its appearance. The cause of multiple renal insufficiency patients caused by acute tubular necrosis varied, can be pided into two categories: one, renal toxic substances poisonous to the kidney, such as drugs, sulfonamides in carbon tetrachloride, mercury, bismuth, agent two chloro sulfonamide (dichlorphenamide); polymyxin antibiotics in hormone, vancomycin, card kanamycin, gentamicin and cephalothin, cefaloridine, neomycin, amphotericin B, and iodine contrast agent, methoxyflurane anesthesia; biological toxins such as snake venom, bee venom, fish mushroom, cantharidin (Cantharidin), can cause acute renal tubular necrosis in the necessary conditions. Two, renal ischemia severe renal ischemia such as severe trauma, extensive burns, surgery, massive hemorrhage, postpartum hemorrhage, severe inflammation, sepsis, shrinkage and electrolyte imbalance, especially with shock, are easily lead to acute tubular necrosis. In addition, intravascular hemolysis (such as blackwater fever and primaquine hemolysis caused by favismand ABO blood transfusion, arsenic poisoning) red blood PRO released, and a large number of trauma (such as muscle crush injury, muscle inflammation) muscle red PRO fluid, through the kidneys, can damage the kidney tubules caused by acute tubular necrosis. The specific pathogenesis of tubular necrosis is not yet fully understood. It happened with the following: 1. The detoxification treatment extremely (usually below 5ml/min, the majority of only 1-2ml/min) the mechanism may be due to the variety of diseases caused by renal ischemia or poisoning, renal tubular epithelial cell injury, the proximal tubular sodium reabsorption is reduced, so that the original in urine sodium and water. When it flows through the distal tubule of the macula densa, stimulate the juxtaglomerular apparatus (juxtaglomerularapparatus) increased in the kidneys release renin, angiotensin II activity caused by glomerular arteriolae contraction, spasm, especially lead to glomerular blood flow decreased outer cortical glomerular filtration rate, extreme reduction. In addition, may also be due to renal ischemia, renal blood perfusion of the afferent arteriole reduced, directly stimulate the juxtaglomerular cell to release renin angiotensin II increased, resulting in contraction of afferent arterioles, detoxification capacity decreased and increased secretion of aldosterone, promote the sodium and water retention. Other scholars believe that the decline in detoxification capacity is due to capillary endothelial damage, swelling, resulting in filtration membrane permeability caused by treatment. The tubular lumen obstruction after injury, necrosis and shedding of renal tubular epithelial cells and inflammatory exudate, blood red (muscle) PRO, into a mass and tube type, the occlusion of the lumen, urine nasty blocked, and oliguria; on the other hand, intraluminal renal capsule swelling, and increase in kidney the pressure, detoxification capacity further decreased. Rupture of renal tubular wall, overflow of original urine. After renal tubular injury, the wall rupture, the tube of the original urine overflow outside the tube, resulting in less urine; at the same time cause renal interstitial edema, increase renal pressure, so that detoxification ability decreased. Some people think that the various disease (shock, trauma, crush injury etc.) caused by acute renal insufficiency induced by renal ischemia reperfusion, the main disease by that occurred after ischemia, renal ischemia and filtration early to reduce or stop (Shao Niao or urine) is a self protective mechanism of kidney, to reduce the burden of reabsorption of renal tubular cells, reduce the oxygen consumption, increase the tolerance to hypoxia, once the renal ischemia were improved (reperfusion), can produce a large number of superoxide anion, cause kidney damage, serious short, acute renal dysfunction is a variety of physiological abnormalities which has the characteristics of comprehensive syndrome, pathogenesis in the course of different periods have different significance. Oliguria after polyuria, renal tubular epithelial begin a new life, at this time due to the pathogenic factors has been lifted, ischemic and toxic substances have been eliminated, blood circulation has been restored; the new tubular epithelial cells still lack the ability to concentrate urine, urine specific gravity is less than 1.015; the metabolites of azotemia and retention the penetrating urination advantage, so hydrouria, called the polyuria stage. Chronic renal insufficiency caused by many diseases, more than half of the blood flow into the kidneys caused by defects, such as the patient because of nausea or diarrhea is too severe, resulting in shrinkage, the result is not enough blood. In addition, heart failure, severe hypotension, cirrhosis or toxic advantage of the kidney drugs may also make kidney blood flow drawbacks. Substances that are toxic to the kidneys can destroy kidney tissue and cause chronic renal failure. There is a common snake venom, fish bile, mushroom and other toxins, tetracycline, gentamicin, kanamycin and amikacin, tobramycin, sulfonamides and other antibiotics, and arsenic, lead, cadmium, carbon tetrachloride, methanol and other chemical toxins. In addition, urinary diseases such as glomerular disease, interstitial nephropathy, or urinary obstruction can develop into renal insufficiency. The kidney is mainly responsible for the regulation of water and electrolyte metabolism, and body wastes such as urea excretion, at the same time it can secrete glucocorticoids, effects of calcium and phosphorus metabolism, and the blood of generation. Kidney function so many and huge, once the kidney suddenly broke, the performance is also ever-changing, very complex.

Contact the Health Information Center

Phone: 0086-15176446195 | TTY: 0086-15176446195 | Email: 763363721wxn@gmail.com | Hours: 8:00 a.m. to 22:00 p.m. China time