Renal artery stenosis - Symptoms.

The symptoms of renal artery stenosis are not very specific; however, if a combination of symptoms is detected, further examination is necessary, especially the use of imaging methods, to confirm atherosclerotic renal artery stenosis.

Arterial hypertension is a mandatory symptom of renal artery stenosis. The features of arterial hypertension typical for atherosclerotic renal artery stenosis include:

• de novo occurrence in old age;
• loss of control over blood pressure, previously reduced with the use of standard antihypertensive therapy regimens;
• refractoriness to combination antihypertensive therapy;
• III degree (European Society of Hypertension, 2003; All-Russian Scientific Society of Cardiologists, 2005) arterial hypertension;
• predominant increase in systolic blood pressure.

Atherosclerotic renovascular hypertension is characterized by prognostically unfavorable variants of the circadian rhythm of arterial pressure, characterized by its insufficient reduction or further increase at night. It is also characterized by more pronounced damage to target organs than in essential arterial hypertension and a higher frequency of associated clinical conditions (cerebral stroke, chronic heart failure). Atherosclerotic renovascular hypertension always belongs to the category of high or very high risk of complications according to the classifications of the European Society of Hypertension (2003) and the All-Russian Scientific Society of Cardiologists (2005).

In atherosclerotic stenosis of the renal arteries, hypercreatininemia is usually detected, usually moderate and therefore erroneously regarded as a sign of "involutional" changes in renal tissue, but sometimes rapidly increasing under the influence of appropriate factors. ACE inhibitors and angiotensin II receptor blockers, as well as NSAIDs, primarily provoke hyperkalemia, often outpacing the growth of serum creatinine levels.

Embolism of intrarenal arteries and arterioles by cholesterol crystals causes rapidly progressive loss of renal function; sometimes diuresis steadily decreases to the point of anuria. Lumbar pain, transient hematuria, and leukocyturia (the pool of leukocytes entering the urine is represented mainly by esosinophils) are possible. As a rule, there is a pronounced and virtually intractable increase in blood pressure with signs of malignancy, including edema of the optic nerve. Signs of embolism of other visceral branches of the aorta often come to the fore in the clinical picture. Cholesterol embolism of intrarenal arterioles can be acute (acute renal failure with anuria, usually irreversible and often fatal), subacute (deterioration of renal function and extrarenal manifestations are not so pronounced) and chronic (repeated embolic episodes causing gradual increase in renal failure). In acute cholesterol embolism, the "general" symptoms are most pronounced, less noticeable in its other forms:

• fever;
• muscle pain;
• weight loss;
• lack of appetite, weakness;
• skin itching;
• acceleration of ESR;
• increased serum C-reactive protein levels;
• hypofibrinogenemia;
• hypereosinophilia;
• hypocomplementemia (not always observed).

Clinical symptoms of embolism of intrarenal arteries and arterioles by cholesterol crystals

Localization of emboli	Symptoms
Arteries of the brain	A headache that is difficult to bear Nausea, vomiting that does not bring relief Disturbances of consciousness Transient ischemic attack/stroke
Retinal arteries	Visual field loss/blindness Bright yellow Hollenhorst plaques on the retina Hemorrhage sites Optic disc edema
Arteries of the digestive organs	"Ischemic" intestinal pain Dynamic intestinal obstruction Gastrointestinal bleeding Gangrene of intestinal loops Acute pancreatitis, including destruction
Renal arteries	Pain in the lumbar region Oligo- and anuria Decreased SCF, hypercreatininemia Hyperkalemia Hematuria, leukocyturia (eosinophiluria)
Arteries of the skin (especially of the lower extremities)	Mesh Livedo Trophic ulcers

Atherosclerotic stenosis of the renal arteries is almost always combined with other manifestations of widespread and often complicated atherosclerosis:

• IHD (including previous acute myocardial infarction, acute coronary syndrome; coronary angiography and/or coronary angioplasty procedures);
• transient ischemic attacks and/or acute cerebrovascular accidents, clinically obvious or asymptomatic atherosclerotic lesions of the carotid arteries;
• intermittent claudication syndrome;
• atherosclerotic lesions of the abdominal aorta, including aneurysm.

Severe coronary artery disease, atherosclerotic lesions of the carotid arteries (including asymptomatic lesions detected by ultrasound Doppler imaging of the carotid arteries), and intermittent claudication syndrome are especially often combined with atherosclerotic renovascular hypertension.

Patients with ischemic kidney disease often have severe heart failure, the treatment options for which are significantly limited due to the impossibility of using RAAS blockers and diuretics in adequate doses. At the peak of a hypertensive crisis in atherosclerotic stenosis of the renal arteries, difficult-to-relieve episodes of pulmonary edema may develop, often recurring.

It is necessary to keep in mind the possibility of a combination of atherosclerotic stenosis of the renal arteries with other chronic nephropathies, especially metabolic (diabetic, urate), considered typical for elderly people (analgesic nephropathy, chronic pyelonephritis), as well as long-standing chronic glomerulonephritis and nephrolithiasis. In this situation, one can suspect ischemic kidney disease based on the features of arterial hypertension (increasing severity in the absence of obvious causes), renal failure (worsening with the administration of ACE inhibitors or angiotensin II receptor blockers in the absence of signs of activity of the underlying kidney disease), as well as a combination of cardiovascular risk factors and signs of the prevalence of the atherosclerotic process.

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