Kidney embolization

While studies of platelet and thrombus accumulation on surfaces have provided important information concerning blood-material interactions, that accumulation is not a direct index of the rate of microemboli generation [e.g., kidney embolism induced by implanted aortic rings often was most severe from rings that remained clean (26, 27)]. Thus, analytical tests that directly quantify microemboli are needed. 

Abbokinase (Urokinase) Pulmonary embolism Human kidney cells... 

The pancreas was first transplanted in 1966. This was a transplant of multiple organs where kidney and duodenum were also transplanted in a 28-year-old woman she exhibited a decrease in sugar levels immediately after transplantation, but died 3 months later due to pulmonary embolism. The first partial pancreatic transplant, in which the donor was a living relative, was performed in 1979 but until 1990, it was considered an experimental procedure. 

Urokinase is also a thrombolytic agent, used for treating pulmonary embolism. Two variants of this protease have already been isolated one of 54 kDa and another of 33 kDa, both displaying proteolytic activity over plasminogen. Until recently, the only exogenous source for this enzyme was urine. However, in 2002 the product called Abbokinase, which is produced in neonatal kidney tissue culture, was approved in the USA. 

Intravenously administered particles with dimensions exceeding 7 /mi (the diameter of the smallest capillaries) will be filtered by the first capillary bed they encounter, usually the lungs, leading to embolism. Intra-arterially administered particles with dimensions exceeding 7 m will be trapped in the closest organ located upstream for example, administration into the mesenteric artery leads to entrapment in the gut, into the renal artery leads to entrapment in the kidney etc. This approach is under investigation to improve the treatment of diseases in the liver. 

In cases of severe fatty liver, there is indeed a risk of fat embolism occurring in the lungs, brain and kidneys. In view of the considerable fat masses stored in the hepatic parenchyma due to this condition, R. Virchow suspected the manifestation of fat embolism as early as 1886. (s. tab. 31.9) Blunt traumatism of the (enlarged) liver with subsequent mobilization of fat is thought to be the cause of this condition. It is not clear at present whether this so-called inundation theory offers sufficient explanation or whether it needs to be amended or even replaced by the so-called segregation theory (high lipaemia, deemulsification of blood fats, etc.). While hepatic fat embolism may be rare, it is nevertheless clinically relevant. 

Of 207 patients with ischemic stroke, stages III or IV, treated with an intravenous infusion of dextran 40 over 4 days, 9 (4.3%) developed acute renal insufficiency attributable to the dextran. Oliguria occurred after a mean time of 4 (range 3-6) days. The incidence of dextran-induced renal insufficiency was higher in patients with pre-existing impaired kidney function. The high risk of death in the patients who developed renal insufficiency was due to non-renal complications, notably pneumonia and pulmonary embolism (10). 

Gupta BK, Spinowitz BS, Charytan C, Wahl SJ. Cholesterol crystal embolization-associated renal failure after therapy with recombinant tissue-type plasminogen activator. Am J Kidney Dis 1993 21(6) 659-62. 

Metabolic studies with I-labeled Ethiodol indicated that the iodized oil was rapidly deiodinated by enzymes in tissues with the iodine appearing as inorganic iodide, which was excreted by the kidney. In humans, no more than 0.5%of the injected iodized oil was found in the blood at any one time, and the urinary excretion was less than 2.5% of the dose per day (159). The most serious side effect of the iodized oils is pulmonary or systemic embolization and granuloma formation (160), which is related to the particle size of the oily drops (150,157), but Kupffer cells can actively capture and phagocytize the iodized oil droplets (161). 

Thrombotic thrombocytopenic purpura—A life-threatening disease involving embolism and thrombosis of the small blood vessels in the brain and kidney. 

De Luis E, Bilbao JI, Garcia-Jalon de Ciercoles JA et al (2007) In vivo evaluation of a new embolic spherical particle Hepasphere in a kidney animal model. Cardiovasc Intervent Radiol, in press... 

Perini S, Gordon RL, LaBerge JM, et al. (1998) Transcatheter embolization of biopsy-related vascular injury in the transplant kidney immediate and long-term outcome. J Vase Intervent Radiol 9 1011-1019... 

It should also be noted that when larger vessels are occluded with coils, collateral arteries form relatively rapidly and the distal vascular bed is still perfused but at a lower pressure than before the embolization. This is the theory behind the proximal occlusion of the splenic artery to halt splenic hemorrhage. The use of these coils presupposes the existence of collaterals. For example, embolization of the renal artery will most likely not result in viable renal tissue as the kidney is an end-organ and will not have a collateral arterial system that will support the kidney. 

Carmignani G, Belgrano E, Martorana G, Puppo P (1978) Clots, oxycel, gelfoam, barium, and cyanoacrylates in transcatheter embolization of rat kidney. Invest Urol 16 9-12... 

I n an experimental animal model, ithasbeen found that after embolization of the kidney, the uterus, or the liver in the sheep with 500-700, 700-900 and 900-1200 pm microspheres that, for each caliber, the level of occlusion was more distal with Contour SE compared to TGMS of the same size [36]. These differences could be explained by a higher intravascular deformation of CSE compared to TGMS (Fig. 10.6.2). There were fewer differences in terms of location between TGMS and Bead Block (Fig. 10.6.2). 

Fig. 10.6.2. In vivo deformation of three types of calibrated microspheres. The length and width of three types of microspheres has been measured on histological slides after embolization of sheep kidneys. The microsphere deformation was calculated by the formula deformation (%) = 100 X (length-width)/width. The graph summarizes the results expressed in boxplots. A view of the deformation of each microsphere type is given below the graph...

Fig. 10.6.5. In vivo detectability of 700-900 pm MR marked microspheres after renal artery embolization in the sheep. The left kidney has been emboli-zed with trisacryl-gelatin microspheres containing an MR marker (L), and the right kidney with control trisacryl-gelatin microspheres (R). MRI study of the explanted kidneys was performed 24 h after embolization (3D SPGR Tl, slice thickness). MR marked microspheres are detectable in the cortical area. No control microsphere is detected in the opposite side...

Fig. 9.11a-f. Renal cell carcinoma in the residual kidney with hemorrhage, medically inoperable, a, b Before and after embolization with PVA and coils, c, d Repeat bleeding 1-1.5 years later pre- and postembolization with PVA, Gelfoam, and coils. e,f Repeat bleeding 9 months later pre- and post-Ethanol embolization. The patient survived for 5 more years before he succumbed to diffuse metastatic disease... 

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