Renal artery stenosis is characterized by a decrease in blood flow through one or both main renal arteries or one of its branches and this condition of stenosis may favor renal artery occlusion, which is characterized either by blockage complete with flow or partial, e.g. of main branches.
Renal artery occlusion may be acute or chronic. Acute occlusion is generally
one-sided. Chronic occlusion can be unilateral or bilateral. Stenosis and
occlusion are generally caused by thromboembolism, atherosclerosis or
fibromuscular dysplasia.
We distinguish 4 conditions of renal infarcion, acute and chronic, massive and
partial flow deficit. In fact, if the embolus is of adequate size it can completely
block the renal artery, but it can also occur the condition in which the flow of
blocks in secondary vessels, e.g. the interlobar arteries.
Thromboembolism is the most common cause. Embolus can originate in the heart
(due to atrial fibrillation, following a myocardial infarction or from
vegetations from bacterial endocarditis) or in the aorta (as ateroemboli); less
commonly, the cause is represented by fat or tumor emboli. Thrombosis of the
renal artery can occur spontaneously or after a trauma, surgery, angiography or
angioplasty. The other causes of acute occlusion include aortic dissection and
rupture of a renal artery aneurysm.
The rapid, total occlusion of large renal arteries for 30-60 min causes a heart
attack. The infarct is typically wedge-shaped and radiates outward from the
affected vessel, so it is called a white infarct, meaning that it affects a
terminal artery, without the possibility of collateral circulation. Symptoms of
acute occlusion include constant and intense pain in the side, abdominal pain,
fever, nausea, vomiting and haematuria. Acute renal damage can develop. Chronic
and progressive stenosis causes refractory hypertension and can lead to chronic
kidney disease. Diagnosis is based on imaging techniques (eg, angio-CT, angio-MR).
Treatment of acute occlusion involves the use of anticoagulants and sometimes
fibrinolytics and / or the use of surgical or catheter embolectomy, or the
combined approach. Treatment of progressive chronic stenosis includes
angioplasty with placement of a stent or with surgical bypass.
About 90% of cases are due to atherosclerosis, which is generally bilateral. Nearly 10% of cases are due to fibromuscular dysplasia, which is usually unilateral. Less than 1% of cases are due to Takayasu arteritis, Kawasaki disease, neurofibromatosis type 1, hematoma of the aortic wall, or aortic dissection. Atherosclerosis develops mainly in patients> 50 years (mostly male) and usually affects the aortic orifice or the proximal segment of the main renal artery.
Chronic progressive stenosis tends to become clinically evident after about 10 years of atherosclerosis, causing atrophy and chronic kidney disease.
Fibromuscular dysplasia consists of the pathological thickening of the arterial wall, most often in the distal part of the main renal artery or in the intrarenal branches. The thickening tends to be irregular and may involve any parietal layer (but most often the average tunic). This disease develops mainly in young adults, especially in women between 20 and 50 years. It is more common among first-degree relatives with fibromuscular dysplasia and patients with the ACE1 gene.
Risk factors that may increase the chances of developing a renal infarction
include:
• Atrial fibrillation - irregular heartbeat
• Previous infarction
• Pulmonary embolism
• Valvular or ischemic heart disease
• Bacterial endocarditis
• Antiphospholipid syndrome
• Polycythemia vera
• Mutation of the V factor of Leiden
• Antithrombin III deficiency
• C and S protein deficiency
Causes and concause of renal infarction
Most renal infarcts occur due to a thromboembolic event, or clots. This
phenomenon can occur in many ways, from disturbances in the mechanisms of
coagulation to physical traumas that lead to the development of clots. The
following are some of the causes of renal infarction:
Due to the obstruction of renal blood flow:
• Renal artery stenosis
• Renal artery embolism
• Atrial fibrillation
• Mitral valve disease
• Oval foramen
• Renal artery thrombosis
• Renal artery aneurysm
• Renal venous thrombosis
Low levels of cardiac output leading to a low blood supply to the kidneys:
• Congestive heart disease
• Hypotension
• Cardiac surgical interventions
The symptoms found during a renal heart failure problem may be non-specific and
is therefore diagnosed later than it should be. Kidney infarction may be the
product of another underlying disease, further confusing the presentation. But
there are a couple of specific kidney related symptoms that are as follows:
• Epigastric pain: largely observed on the epigastric dermatoma and often
irradiated in the lower back or on the right or left side depending on the
affected side.
• Pain in the side: experience as a very severe excruciating pain located on the
side. The pain radiates in the lower back or on the left or right side.
• Painful abdomen, sometimes not treatable :: when the abdomen is palpated in
the upper areas, one can appreciate intense pain on the epigastrium. This
abdominal pain is not associated with pain of protection or rebound.
Often, when the renal infarction occurs in an acute way, it is in the emergency
room because of the patient who feels a strong pain in the lumbar and abdominal
area. Once a brief history and a physical examination have been performed, the
imaging tests will confirm that a renal infarction has actually occurred. Below
are some tests that could be performed in a suspected case of renal failure:
• CT scan or MRI scan: provides a detailed look at the arteries supplying the
kidneys
• Urinalysis: will help determine if blood is present in urine and in proteins
and white blood cells
• Blood test: check if all blood values are in normal values, looking for
signs of anemia
• Doppler ultrasound: may be able to detect any calcifications or renal
aneurysms
• Electrocardiogram and echocardiogram: used to visualize the electrical
activity of the heart for the diagnosis of abnormalities in the function and to
directly visualize the images of the heart, respectively.
• General principles: since those with kidney problems often have high blood
pressure, prescription of antihypertensive drugs is often required. High blood
pressure caused by increased renin that occurs in renal failure. If
thromboembolism is suspected to be a risk, the use of anticoagulant therapy may
be justified. If the kidney atrophy has not yet occurred, reperfusion therapy
should be considered.
• Diffuse atherosclerotic disease and atrial fibrillation
• Anticoagulation: commonly implemented via intravenous heparin followed by oral
warfarin. Heparin is then stopped once the INR is stable and continues with
warfarin. The INR target is to prevent renal infarction due to a clot between
2.0 and 3.0. However, this interval may need to be changed depending on the
cause.
• Percutaneous endovascular therapy: a procedure that directly opens blood
vessels in the kidney to increase perfusion. It can be used for thrombolysis,
thrombectomy and / or angioplasty with or without stent placement.
• Thrombolysis and thrombectomy: treatments to dissolve dangerous clots or to
surgically remove a dangerous clot, respectively.
• Angioplasty: a procedure that opens the blocked blood vessel with or without
stent placement. This can help improve blood pressure.
• Surgery: often reserved or severe cases of renal infarction such as in
patients with traumatic renal artery occlusion and embolic renal artery
occlusion. This involves the surgical removal of the obstruction.