Pathology of renal artery disease

2021-01-26 12:00 AM

Progression of atherosclerotic lesions leading to renal artery stenosis occurs in about 50% of cases, of which nearly 20% is complete obstruction of the renal artery.


Renal artery disease includes damage to the renal artery, possibly in the large renal artery, and possibly in small and medium scale. It can be primary (congenital injury) or secondary to another disorder. The course of renal artery disease can be acute or chronic. The main clinical manifestation of renal artery disease is hypertension. Confirming diagnosis still must be based on subclinical tests, especially renal artery.

Renal arterial hypertension is a secondary type of hypertension. The incidence of this disease is still difficult to determine because not all conditions with damage to the renal artery cause hypertension. In the population of non-selective hypertension, renal artery disease causes only less than 1%.


Renal artery disease can be classified according to the cause, the course of the disease or the location of the damage in the renal artery. Below we would like to mention only two commonly used classifications: stool by cause and by course of the disease.

Sort by cause

Depending on the cause, renal artery disease is divided into 2 categories

Congenital diseases of the renal artery:

Common in young people include:

Congenital renal artery atrophy.

Renal artery aneurysm.

Ventilation - renal vein.

Kidney prolapse and tuberculosis.

Aortic stenosis above the renal artery origin.

Pathologies of secondary renal artery damage:

Renal atherosclerosis.

Renal artery fibrosis dysplasia.

Renal artery obstruction.

Takayasu’s disease 

Classification according to the course of the disease

Depending on the course of the kidney artery disease is divided into two types of rapid (acute) or slow (chronic), note that some causes can be progressive or chronic depending on the context (e.g., e.g.: embolism due to cholesterol crystals).

Acute or rapidly progressing renal artery diseases:

Diseases of thrombotic vessels (glomerular capillaries and arterioles).

Malignant renal vascular fibrosis (blood vessels in the kidneys of all sizes).

Cholesterol embolism (small artery in the kidney).

Peri-artery macular inflammation (medium-sized arteries).

Acute scleroderma (blood vessels in the kidneys of all sizes).

Renal artery diseases progress in a chronic fashion:

Renal artery stenosis.

Cholesterol embolism.

Benign renal vascular fibrosis.

Antiphospholipid syndrome.

Chronic transplant rejection of kidney transplantation.


(Secondary kidney artery stenosis is covered here.)

Renal atherosclerosis

The most common cause of hypertension due to renal vascular disease (accounting

2/3 cases). This is the pathology seen in adults after 45 years of age. Narrative atherosclerotic lesions usually appear at the hole originating from the renal artery from the aorta or in the first 1/3 of the renal artery. Atherosclerotic lesions can be found in other arteries such as arteries in the extremities, coronary arteries, carotid artery ...

Progression of atherosclerotic lesions leading to renal artery stenosis occurs in about 50% of cases, of which nearly 20% is complete obstruction of the renal artery.

Renal artery fibrosis dysplasia

Accounting for 25% of the causes of hypertension in renal artery disease. Common is dysplasia in the middle layer of the artery. This pathology is seen mainly in young women before 40 years old. Damage to the renal artery is usually seen at 2/3 far away from the base or in the dividing branches of the renal artery, forming a succession of narrow segments and dilatations (rosary markers on renal angiography). This fibrosis dysplasia can also be found in other arteries such as the carotid artery and the pelvic artery. Other types of dysplasia such as endothelial hyperplasia, fibrosis of dysplasia around the middle layer are very rare.

Other blood vessel damage

It may be rare in the renal artery such as aneurysm, thrombosis, dynamic - venous aperture, arteritis, squeezing from the outside (due to the tumour in the abdomen, adrenal medullary tumours).


The pathophysiology of renal artery hypertension was known in dogs by Goldblatt in 1934: by incompletely constricting the renal artery, causing hypertension, and this increase ceased to exist. again, when the renal artery is opened.

In people with 2 types of renal artery stenosis: unilateral renal artery stenosis with normal opposite kidney and 2-sided renal artery stenosis or unilateral renal artery stenosis on 1 single kidney.

Unilateral and opposing renal artery stenosis is normal:

When the degree of renal artery stenosis is not much, the decrease in renal perfusion pressure is moderate and the proper functioning of the réninic system - angiotensin will correct renal hemodynamic disorders, so there may be no symptoms. clinical evidence.

When the renal artery narrowed in a large degree, the compensation in the kidney will not be enough to normalize renal hemodynamic, so renal perfusion will decrease and stimulate the rénin system - angiotensin frequently increases angiotensin II. leads to constriction of the common arteries and increases blood pressure. In addition, there is also a mechanism of secondary aldosteronism and increased release as well as increased effects of noradrenalin secondary to activation of the rénin-angiotensin system.

Hypertension occurs only when the degree of narrowing is severe, reducing the renal artery aperture from 70 to 80%.

In the opposite kidney without artery stenosis, there will be an increase in the pressure in the kidney leading to increased sodium excretion by this kidney (called hypertension), but this renal secretion is greatly reduced.

In the kidneys with stenosis, there is increased secretion of rénin, decreased sodium excretion, increased Angiotensin II in the kidney causes constriction of the glomerular arteries (self-regulation) contributes to glomerular filtration of Narrow kidney.

The use of ACE inhibitors prevents the formation of Angiotensin II thereby lowering arterial blood pressure. But for the kidneys with artery stenosis, it causes loss of self-regulation, the glomerular filtration rate is reduced, and for the kidneys without artery stenosis, the glomerular filtration rate and renal blood flow do not change or increase.

With long-term renal artery stenosis, surgery may no longer reduce blood pressure, due to damage to the arterioles secondary to hypertension in places where the arteries are not.

Bilateral artery stenosis or unique renal artery stenosis:

In this situation, a decrease in arterial perfusion is associated with all kidney damage. Here there is no normal opposite kidney to limit hypertension and increase volume. Since increased blood volume reduces renin secretion, hypertension depends in part on the increase in blood volume to the kidneys.

Angiotensin II plays a very important role in maintaining kidney function. Therefore, the use of Angiotensin II Reduced ACE inhibitors can lead to a severe decrease in glomerular filtration rate and acute renal failure.

Clinical symptoms

The most important clinical manifestation of renal artery stenosis is hypertension. The problem is that before a patient with hypertension, to distinguish whether this is primary hypertension or hypertension due to renal artery stenosis. Several studies comparing large numbers of primary hypertension and renal artery stenosis have shown no significant symptoms to help distinguish between the two.

However, there is also some data through questioning, clinical examination and follow-up treatment of hypertensive patients, which in turn allows the suggestion of renal vascular disease including the following factors:

The onset of hypertension at age under 30 or over 55 with severe hypertension.

Sudden hypertension or worsening of blood pressure with good treatment.

A systolic murmur is detected in the epigastric region or at the side of the navel and especially a continuous blow.

Detection of impaired renal function or urinary abnormality (proteinuria, microscopic haematuria) prior to antihypertensive therapy.

Ineffective with beta-blockers, diuretics, vasodilators (hydralazine) and calcium inhibitors.

Impaired renal function when using ACE inhibitors.

In renal artery stenosis, blood pressure values ​​are usually very high, with manifestations of secretory, papillary oedema at wick microscopy. But a small or moderate increase in blood pressure can also be seen in renal artery stenosis.


The definitive diagnosis of renal artery disease is usually based on renal angiography. Currently, the use of numbering techniques allows reducing the number of contrasted iodine derivatives injected into arteries.

Renal artery colour Doppler ultrasound: allows to evaluate the position of stenosis, the degree of stenosis, the number of stenoses, the condition of the renal artery anterior and posterior stenosis (dilatation, aneurysm, atherosclerosis, ...). It is the preferred test because it is non-invasive, it is inexpensive, and has relatively high sensitivity and specificity.

Minute intravenous contrast nephrology with early film at a first and fifth minute after injection is commonly used. The unilateral decrease in kidney size, delayed excretion, a slow increase in concentration (very beautiful picture) are indications of unilateral renal vascular disease but the percentage of false positives and false negatives of This method is quite advanced.

Nephrography with radioisotope with DTPA or Hippuran marker allows the study of filtration asymmetry, which is also no more sensitive than other methods.

Peripheral venous blood renin activity measurement: is not an orientation test because the sensitivity is low (57%) and the specificity is not high (66%). Serum rénin increases by 15% of primary hypertension and is normal in more than 20% of hypertensive cases due to renal artery disease.

In general, there is currently no non-invasive test that can rule out a diagnosis of nephrotic hypertension, if the results of these tests are negative. The clinical signs are still valid to help decide whether to perform a renal artery to confirm hypertension caused by renal artery disease.

Determination of renin in 2 blood samples of 2 renal veins (rate 1.5) is also valid evidence. But a good treatment result can be achieved in 50 to 75% of cases when the ratio is below 1.5, so this test also has its limitations.

Today, people still do research on kidney scintigraphy with DPTA and or Hippuran before and after using ACE inhibitors. In the case of renal artery stenosis noted after using ACE inhibitors, there is a disturbance of renal excretion function compared to the benign side.

In bilateral renal artery, stenosis diagnosis is often difficult. Often patients with very severe hypertension that are difficult to control, impaired renal function are common. Acute renal failure that occurs with ACE inhibitors strongly suggests bilateral renal artery stenosis, with only renal angiography confirming the diagnosis.

Gu D. et al have studied the methods of imaging exploration of renal artery stenosis and have conclusions about the sensitivity and specificity of each method according to the following table (2002).

Table: Sensitivity and specificity of the probe.




Kidney artery scan






Magnetic resonance imaging






CT-Scanner (with Captopril)






Renal artery Doppler ultrasound





Numbered angiography (intravenous)



UIV movie soon



In summary, the definitive diagnosis of renal artery stenosis is largely based on imaging exploration, in which renal angiography still plays a decisive role. The only clinically suggestive and the most popular non-invasive test to date is the renal artery Doppler ultrasound.


Treatments applied in renal artery disease

The ideal treatment is to heal arterial hypertension by repairing the artery damage caused by kidney anaemia. This correction can be done by surgical intervention or by percutaneous angioplasty (percutaneous angioplasty). Current drug therapy can normalize blood pressure, but drugs have no effect on the cause of renal artery disease.

Drug therapy:

ACE inhibitors are often used, in combination with diuretics, beta-blockers, and calcium inhibitors.

Hypertension is usually well controlled with a combination of drugs in most cases. Note that the use of drugs, especially antihypertensive drugs of ACE inhibitors can impair the self-regulation of the kidneys, reduce glomerular filtration, so it is necessary to check kidney function regularly. take this group of drugs. In the case of bilateral renal artery stenosis, the ACE inhibitor group is contraindicated.

Surgical treatment:

With the aim of excluding artery damage or anaemia consequences. It is possible to intervene by dissecting the endothelium, bridging the artery or directly cutting the lesion depending on the location, extent of the damage as well as the condition of kidney failure to decide on the method of choice.

Treatment of percutaneous angioplasty:

Allow dilating the narrowed artery. Has been used for nearly 20 years now, is increasingly widely adopted. The advantage of this method is that the procedure is gentle, the post-operative time is short, the results are very good.

Choosing which treatment is appropriate for the patient should take into account the patient's age, the severity and location of the blockage, atherosclerosis elsewhere, and the effects of atherosclerosis. organs.

In the case of renal vascular dysplasia, which is common in young people, orthopaedics or surgery are the methods of choice because they often give good results, allowing for the healing of hypertension.

In cases of atherosclerosis, surgery or orthopaedic vascular surgery, it is necessary to consider carefully because complications, especially reduced kidney function already exist, the assessment of remaining kidney function is the decisive factor for choosing. choose treatment.

Treat the specifics of each cause

Thrombotic microvascular diseases:

Treat the cause.

Use fresh plasma during plasma filtration.

High-dose corticosteroid therapy.

The prognosis of survival depends on the cause, the mortality rate is about 30-40%.

Malignant renal vascular fibrosis:

This is an emergency treatment. Purpose:

Control of blood pressure: Treatment is often used.

Intravenous nicardipine (Loxene) 1 - 10mg / hour.

Intravenous labetalol (Trandate) 0.5 - 1 mg / min.

And inhibition of oral ACE inhibitors after volume normalization.

Blood volume control: Assessment of blood volume is needed:

In the case of hypovolemia; Quick adjustment with normal saline solution. Contraindicated to use urinary drugs.

In left ventricular failure, loop diuretics should be used.

Usually during the first-month kidney function is damaged (aggravated by decreased perfusion) and sometimes dialysis is required. Renal function gradually improves and can return to normal if blood pressure is well controlled (<130/80 mmHg).

Cholesterol embolism :

Symptomatic treatment is primary (anticoagulant discontinuation, blood pressure control, dialysis).

Corticoid therapy is often used, which increases survival.

The prognosis is generally bad: Death of more than 40% after 6 months.

Inflammation around the nodular artery:

Perivascular nodular inflammation is not associated with viral hepatitis: steroid therapy sometimes requires cyclophosphamide or Azathioprine in severe forms.

In cases associated with hepatitis B: antiviral therapy (Lamivudine) in combination with corticosteroids.


Acute kidney damage: Malignant hypertension with the haemolytic syndrome and hyperuricemia.

Emergency treatment with hypotension especially ACE inhibitors.

Renal artery stenosis:

Narrow due to fibrous dysplasia: percutaneous renal angioplasty is an option. Allow healing blood pressure in 70 - 90% of cases. The narrow back is rare.

Atherosclerotic stenosis: 2 therapeutic purposes are: control blood pressure and preserve kidney function. Renal artery repair with orthopaedic or surgery is indicated when:

Kidney size> 8 cm on the side of the artery stenosis.

Severe hypertension, resistance to treatment, with pulmonary oedema, kidney failure.

Narrow over 75% of the renal artery lumen.

2-sided stenosis or 1 side on a single kidney.

Benign renal vascular fibrosis:

There is no specific treatment, treatment includes:

Treatment of hypertension: It is necessary to combine 2 drugs, including an ACE inhibitor (protect the kidneys).

Repair of cardiovascular risk factors.

Slowing the progression of chronic renal failure: note that good treatment of hypertension and anaemia (if any) are the two main factors that help patients maintain stable kidney function over the long term.

Treatment of complications of chronic kidney failure.