The mechanism behind<unk>  is no different from other types of blood clots in other parts of the body. Rudolf Virchow, was the first to describe the physiological mechanism behind venous<unk>  (blood clots) using three related factors, known as Virchow's Triad; damage to the blood vessel (endothelial damage), decrease in blood flow (stasis) and increased coagulability of the blood (thrombophilia or hypercoagulability). it is possible for one of these factors alone to cause a blood clot, but in most cases, a combination or all of these factors induce the formation of a blood clot. Decreased urine output or kidney function may be the only observable symptoms caused by a blood clot<unk> <unk> . Other less common causes include hypercoagulable state, invasion by<unk>  cell carcinoma, kidney transplantation, Behcet syndrome, antiphospholipid antibody syndrome or blunt trauma to the back or abdomen.<unk>  tissue damage Damage to the endothelial tissue of the<unk>  can be caused by blunt damage, trauma during venography, a<unk>  transplant, tumors, acute rejection, vasculitis or spontaneous micro-trauma to the endothelium due to homocystinuria. Cystathionine beta synthase deficiency, also known as homocystinuria, is an autosomal recessive inherited disorder in which the body is not able to process certain building blocks of proteins correctly due to a mutation to the CBS gene. This mutation causes the amino acid homocystine not to be used properly thus high levels build up in the blood, damaging the endothelial tissue and increasing the likelihood of<unk> . Decreased blood flow The most common cause of<unk>  in infants is dehydration. Dehydration may be caused by reduction in both volume and circulatory blood volume due to water depleting abnormalities like diarrhea or vomiting. The decrease in blood volume due to dehydration will cause blood flow to be diverted away from the kidneys to other organs, resulting in slower blood flow to the kidneys, increasing chances of a blood clot occurrence. "RVT is known to occur in the absence of clinically obvious shock e.g. following neonatal distress and placement of central venous catheters."<unk>  can also be induced by post transplant distortion or physical distortion or compression of the<unk> <unk> , which depending on the shape distortion can affect the rate of flow through the<unk> . Hypercoagulability Hypercoagulability is an abnormality of the blood that increases the risk of the formation blood clots. Nephrotic syndrome patients have a higher risk of<unk>  development due to hypercoagulability caused by proteinuria. The increased loss of proteins in the urine caused by nephrotic syndrome results in lower osmotic pressure. Reduced osmotic pressure will trigger the liver to produce more proteins like fibrinogen and beta-thromboglobulin, which promote blood clotting. Other than nephrotic syndrome, there are many other factors that can promote hypercoagulability. Hypercoagulability can be promoted by increased platelet count, enhanced platelet aggregation, increased protein S count, and a decrease in coagulation inhibiters like antithrombin. Hypercoagulability can be inherited and/or acquired. Hyperhomocysteinemia, a condition known to promote clots, can be caused by a combination of genetic factors and vitamin B6, vitamin B12 and folic acid deficiency. Factor V Leiden and mutations of the prothrombin gene are the two most common genetic causes of hypercoagulability. About 5% of the general population have these heterozygous mutations and in the thrombophilic population, 45–63% have these mutations. Membranous glomerulonephritis The incidence of<unk>  in people with Nephrotic syndrome ranges from 5% to 65%. Nephrotic syndrome is caused by membranous glomerulonephritis, minimal change disease, and focal segmental glomerulosclerosis.
Renal vein thrombosis
Pyelonephritis
Pyonephrosis
Hydronephrosis
Glomerulonephrosis
Glomerulonephritis
Obstructive uropathy
Ureteral cancer