Renal Vein Thrombosis
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Renal Vein Thrombosis
Renal vein thrombosis develops when a blood clot forms in the renal vein, which carries blood from the kidneys back to the heart. The disorder is not common.
Renal vein thrombosis occurs in both infants and adults. Onset of the disorder can be rapid (acute) or gradual. The number of people who suffer from renal vein thrombosis is difficult to determine, as many people do not show symptoms, and the disorder is diagnosed only by specific tests. Ninety percent of childhood cases occur in children under one year old, and 75% occur in infants under one month of age. In adult women, oral contraceptive use increases the risk of renal vein thrombosis.
Causes and symptoms
In children, renal vein thrombosis almost always occurs rapidly after an episode of severe dehydration. Severe dehydration decreases blood volume and causes the blood to clot more readily.
In adults, renal vein thrombosis can be caused by injury to the abdomen or back, as a result of malignant kidney tumors growing into the renal vein, or as a result of kidney diseases that cause degenerative changes in the cells of the renal tubules (nephrotic syndrome).
Acute onset of renal vein thrombosis at any age causes pain in the lower back and side, fever, bloody urine, decreased urine output, and sometimes kidney failure. In adults, when the onset of the disorder is gradual, there is a slow decrease in kidney function, and protein appears in the urine. Many adults with renal vein thrombosis show few symptoms.
Renal venography, where a contrast material (dye) is injected into the renal vein before x rays are taken, is one of the best ways to detect renal vein thrombosis. Other useful tests to detect a clot include computed tomography scans (CT scans), magnetic resonance imaging (MRI), and ultrasound.
One of the major goals of treatment is to prevent the blood clot in the renal vein from detaching and moving into the lungs, where it can cause serious complications as a pulmonary embolism. The enzyme streptokinase may be given to help dissolve the renal clot. Anticoagulant medications are usually prescribed to prevent clots from recurring. Rarely, when there is a complete blockage of the renal vein in infants, the kidney must be surgically removed.
Most cases of renal vein thrombosis resolve without any permanent damage. Death from renal vein thrombosis is rare, and is often caused by the blood clot detaching and lodging in the heart or lungs.
There is no specific prevention for renal vein thrombosis. Preventing dehydration reduces the risk that it will occur.
National Kidney Foundation. 30 East 33rd St., New York, NY 10016. (800) 622-9010.http://www.kidney.org.
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pertaining to the kidney. See also kidney.
results from infected emboli and infarcts. Usually without localizing signs unless they are very large and palpable, or when they extend into the renal pelvis and cause pyelonephritis.
rare, incidental necropsy finding.
failure of the renal tissue to develop; unilateral agenesis causes compensatory hypertrophy in the single kidney; bilateral is fatal. Commonly accompanies genital tract malformation.
see Table 9.
avian renal hemorrhage
sporadic unexplained disease of turkeys; sudden death is common.
is conducted usually with a biopsy needle introduced percutaneously through the flank. In food animals it is possible to fix the left kidney via a rectal manipulation, but the right kidney can be impossible to reach.
renal capsular cyst
see feline perirenal cysts.
commonest in old male dogs. They are very large, spread locally and metastasize widely.
see urinary cast.
renal clearance tests
renal cortical fissures
external fissures created by the lobar structure of the large ruminant kidney.
renal cortical hypoplasia
see renal dysplasia (below).
renal cortical necrosis
results from patchy or complete renal ischemia and is part of the terminal state of many diseases, e.g. severe metritis, grain overload in cattle, azoturia in horses.
renal countercurrent system
incidental necropsy finding except for polycystic kidney disease. See also feline perirenal cysts.
inherited as an autosomal dominant trait in middle-aged German shepherd bitches with generalized nodular dermatofibrosis.
renal diabetes insipidus
see nephrogenic diabetes insipidus.
diverticuli of the renal pelvis.
reduced capacity to excrete metabolic products which accumulate systemically and are detectable clinicopathologically by renal function tests. The early stage of uremia.
small, misshapen kidneys at birth. May be caused by intrauterine infection of the fetus by virus, but numerous inherited renal dysplasias occur in dogs. They occur in several breeds and are manifested by signs of chronic renal insufficiency, e.g. polyuria, polydypsia, poor growth and weight gain, pale mucous membranes, and renal secondary osteodystrophia fibrosa, from an early age.
renal erythropoietic factor
inability of the kidney to maintain normal function. Impairment of kidney function affects most of the body's systems because of its important role in maintaining fluid balance, regulating the electrochemical composition of body fluids, providing constant protection against acid-base imbalance, and controlling blood pressure. See also kidney.
renal function tests
include blood urea nitrogen and serum creatinine estimations, tests of concentrating ability, tests of ability to excrete test substances, e.g. phenolsulfonphthalein (PSP) clearance test. Of the urine tests, only specific gravity (SG) has any significance in terms of a function test but abnormalities of urine should lead to a function test being conducted.
a fissure on the medial border of the kidney through which arteries, veins and ureter enter.
renal hypophosphatemic rickets
inherited as an X-linked dominant trait in children and mice; characterized by hypophosphatemia and normocalcemia due to failure of phosphate resorption in renal tubules, and skeletal deformities. Called also vitamin-resistant rickets.
results from embolic or thrombotic occlusion of renal arteries or branches. Clinical signs are those of renal colic initially followed by toxemia if the infarct is infected.
see renal dysfunction (above).
a significant cause of renal dysfunction and cortical and medullary necrosis. Is usually part of a general state of shock, dehydration and severe toxemia.
a large mass of a kidney, comprising the tissue contributing to each pyramid; kidneys may be unilobar (unipyramidal), e.g. cats, dogs, small ruminants, horses, or multilobar (multipyramidal), e.g. cattle, pigs.
small masses of kidney tissue comprising a medullary ray and its associated nephrons.
renal medullary necrosis
necrosis of the renal medulla due to restriction of blood flow in medullary vessels, usually due to venous occlusion.
renal medullary washout
see medullary solute washout.
renal osteodystrophy, renal osteitis fibrosa, renal osteitis fibrosa cystica
see renal secondary hyperparathyroidism.
deposition of oxalate crystals in renal tubules of patients poisoned by dietary oxalate, usually in poisonous plants.
see renal papilla.
renal papillary necrosis
necrosis of renal papillae due usually to obstruction to urinary flow or poisoning or dehydration.
the chamber in the kidney into which the collecting tubules discharge urine and from which urine is voided into the ureter.
renal plasma flow
the effective rate of blood flow through the kidneys; the determining factor relative to the rate of glomerular filtration.
renal portal system
a system unique to birds; half to two thirds of the blood supply to the kidney comes from the hindlimbs via veins and terminates in peritubular capillaries where it is mixed with arteriolar blood coming from the glomeruli.
see renal secondary hyperparathyroidism.
cessation of the excretory function of the kidney; oliguria.
renal spongiform encephalopathy
spongiform encephalopathy associated with renal failure.
renal tubular casts
see urinary cast.
renal vein thrombosis
commonly associated with renal amyloidosis in dogs.