renovascular hypertension
Introduction
Introduction to renal vascular hypertension Renal vascular hypertension (renalvascularhypertension) is a common secondary hypertension. The stenosis of one or both renal arteries and their branches caused by various causes can progress to a certain extent, which can cause renal vascular hypertension. Blood pressure can be restored to normal or improved after intervention or surgery. This disease can lead to ischemic nephropathy and end stage renal disease, which is different from renal arteriosclerosis caused by essential hypertension. basic knowledge The proportion of the disease: in patients with nephritis, the incidence of this disease is about 1-2% Susceptible people: no special people Mode of infection: non-infectious Complications: hemorrhagic disease hemophilia myocardial infarction heart failure
Cause
Causes of renal vascular hypertension
(1) Causes of the disease
Renal vascular hypertension can be caused by various diseases that can cause renal artery stenosis or embolism. Common causes include:
1 The first place in China is aorto-arteritis (AA), which may be an autoimmune disease triggered by infectious factors, mainly involving the middle layer of the artery, and the outer membrane and intima are also violated.
2 atherosclerosis (AS) is a systemic disease, more common in people over the age of 50, often involving the beginning of the renal artery, AS is the most common cause in Western countries, accounting for 60% to 70%, domestic incidence There is an upward trend.
3 arterial fibrosis dysplasia (FMD) or fibromuscular hyperplasia (fibromuscular hyperplasia), is an embryonic viral infection (rubella) or congenital midline myocyte developmental disorder, manifested as arterial intima or mid-central or Eccentric fibrous tissue hyperplasia, lesions located in the distal 2 / 3 of the renal artery, often with multiple stenosis, more common in women under 40 years of age, often accompanied by hypokalemia, the domestic account of the second cause of RVH, about 20% .
4 other reasons, such as arterial anastomotic stenosis after renal transplantation, renal artery injury, renal aneurysm, intrarenal or perirenal causes of renal artery trunk or branch stenosis, renal arteriovenous fistula (congenital or acquired) stealing Blood (split), the above causes renin-angiotensin-aldosterone (RAAS) system activation and kallikrein-kinin-prostaglandin system (KKPS) antagonizes the attenuation of RAAS system, and may have a common atrial natriuretic peptide Role causes high blood pressure.
In 1906, Janeway caused hypertension in one side of the dog's renal artery for 105 days, but did not study it further; it was not until 1934 that the Goldblatt experiment caused an animal model of renal ischemic hypertension that it regained attention. Thereby laying the theoretical foundation of renal vascular hypertension.
The mechanism of hypertension in renal artery narrowing is not fully understood. It is generally believed that the reduction of renal blood flow leads to a condition of renal deficiency, but some people find it mildly before and after renal artery narrowing. Or when the renal artery is narrowed, the decrease of renal blood flow is only temporary. With the establishment of the collateral circulation, the renal blood flow can return to the normal range. Some people make the animal breathe less oxygen or Perfusion of the kidney with venous blood does not produce hypertension. Therefore, renal ischemia and hypoxia are factors that contribute to renal vascular hypertension, but other conditions exist.
There are several arguments in the literature regarding the pathogenesis of renal vascular hypertension. Currently, there are three types that are generally accepted:
First, the kidney's boost system
Renal-angiotensin-aldosterone system, the RAA system, renin is a proteolytic enzyme with heat-labile and non-dialysis properties. Renin itself is not Vasopressin must be combined with 2 globulin produced in the liver (also known as renin activin or hypertonin or hypertonicogen, which contains a substrate that can be acted upon by renin). The molecular structure of the renin substrate acts to cleave at the 10th and 11th leucine junctions, releasing the decapeptide into angiotensin I (AI), and no angiotensin I The boosting effect, when it flows through the vascular bed of each organ, especially in the pulmonary circulation, the invertase breaks between the 8th and 9th positions of the molecular structure, releasing the octapeptide and becoming angiotensin II (AII), which is A potent vasoconstrictor, recently proposed to remove a first amino acid from angiotensin II and then aminotranspeptidase to release a heptapeptide called angiotensin (AIII), which stimulates the secretion of aldosterone. Several times stronger than angiotensin II, blood vessels The role of angiotensin II to III:
1 directly shrink the blood vessels; 2 indirectly contract the blood vessels through the sympathetic nervous system;
3 contraction output small arteries and the input arterioles do not contract, thereby increasing glomerular pressure and reducing sodium discharge;
4 stimulate the adrenal cortex to secrete aldosterone. The half-life of angiotensin II and III in the blood circulation is only a few minutes. After degradation, small molecules of inactive product amino acids, dipeptides and tripeptides are formed. Therefore, the maintenance of hypertension depends on adrenaline. And the role of aldosterone.
In addition to producing renin, the kidney also produces hypertensive proteases, which have the effect of decomposing angiotensin. Under normal conditions, the two maintain equilibrium without causing hypertension, such as renal ischemia, hypoxia, and renin. Increased secretion, thereby destroying the normal balance, producing too much angiotensin and causing high blood pressure.
Experiments have shown that the kidney can play a role in the secretion of aldosterone. Angiotensin II and III can stimulate the secretion of aldosterone, which indicates that hypertension produced by angiotensin II and III, on the one hand, shrinks the arterioles and increases the circumference. Resistance; on the other hand, the increase in aldosterone secretion promotes the retention of sodium and water, increasing the capacity of the extracellular fluid, thus forming a renin-angiotensin-aldosterone system.
Second, the system of kidney regulation of high blood pressure substances
In the near future, many experiments have shown that in addition to the above-mentioned renin-angiotensin-aldosterone system, another system for regulating blood pressure, kallikreinkinin-prostaglandin system (KKP system) has been discovered. ).
1. Renal kallikrein-kinin system The kinin is converted from the kallikrein of the liver by the kallikrein produced by the kidney. The kallikrein of the kidney is more than 90%. Distributed in the cortex, the medulla is 4.5% and the nipple is 4.1%. The active enzyme of kinin in the cortex is only 1.5%, and the main site may be in the juxtaglomerular, kallikrein activity. The higher the catalytic kininogen hydrolysis, the more kinins are produced. In addition, the kidneys can secrete kinin hydrolase, which can destroy the kinins produced.
Renal kinins are currently considered to have the following effects:
1 promote small artery relaxation, so that peripheral vascular resistance decreased;
2 renal arteriolar relaxation, increased renal blood flow, improve renal cortical ischemia;
3 promote sodium, water discharge, water discharge more than sodium, so urinary osmotic pressure decreased, water, sodium discharge increased resulting in decreased plasma volume, blood hematocrit and plasma total protein concentration increased;
4 Because of the decrease in peripheral resistance of the blood vessels and the decrease in circulating blood volume, blood pressure can be lowered, so there is an antihypertensive effect.
The above effects are mainly caused by the promotion of prostaglandin by kinins, but some of them are direct effects of kinins.
2. The prostaglandins of the kidney have been detected in a variety of prostaglandins, and three prostaglandins that can be isolated in the renal medulla, namely PGE2, PGA2, and PGF2, have low levels of prostaglandins in the renal cortex. The medulla has a higher content of nipples, and the amount of PGE2 in the kidney is less, mainly PGA2 and PGF2, which are generally not stored in the cells. Once synthesized, they are released, and they are transferred to the cortex through the intrarenal circulation to exert physiological benefits. Another part of PGE2, PGF2 is destroyed by lung tissue through the renal vein into the systemic circulation, and PGA2 can exist in the systemic circulation.
The role of renal prostaglandins:
1 renal artery perfusion PGE2 can cause local vasodilation, increase renal blood flow;
2 prostaglandins can also redistribute renal blood flow, even if the medullary blood flow declines and the intradermal blood flow increases;
3PGE2 and PGA2 can cause renal glomerular artery relaxation, which increases the capillary pressure around the proximal convoluted tubules, thus reducing the reabsorption capacity of the proximal convoluted tubules to water and salt. PGA2 and PGE2 can inhibit Na+-K- on the tubular membrane of renal tubules. - The activity of ATPase makes the intracellular Na+ not easy to run into the fluid around the renal tubules, affecting the reabsorption of sodium and water by the renal tubules, resulting in diuretic effect. PGE2 can also inhibit vasopressin and increase urine output. Promote the excretion of sodium, potassium and water. Kidney prostaglandins also antagonize the use of catecholamines, but can not inhibit the secretion of catecholamines. Therefore, the adenine-prostaglandin system has the effect of regulating the increase of renin, which is caused by angiotensin to promote aldosterone secretion. Increased, the latter can increase the secretion of prostaglandin releasing enzyme, thereby accelerating the synthesis of prostaglandin PGA2, PGE2.
Third, to renal hypertension (renoprival hypertension)
Renal hypertension refers to hypertension caused by non-function of kidney tissue. It can also be called renal deficiency hypertension or post-nephrectomy hypertension. In addition to antihypertensive substances, the kidneys also regulate body fluids. The function of the electrolyte and the effect of excreting the body's boosting factor, the clinically seen hypertensive patients discharge more water and sodium than normal people, and the water discharge is relatively more, so the proportion of sodium in the body is increased, in another On the one hand, the occurrence of high blood pressure is generally seen in the body's increased water, blood loss can be reduced after water loss, blood pressure after a large number of infusions, more obvious in uremic hypertensive patients, such patients have more retention of sodium and water Sensitive, animal experiments have also confirmed a similar phenomenon, a large reduction in renal tissue can make animals sensitive to high-salt diet; high salt intake after double nephrectomy can cause renal hypertension, therefore, kidney tissue completely loses function like double nephrectomy Similarly, the high blood pressure that occurs is significantly related to the imbalance of body fluids and sodium salts. In addition, the body's boosting substances cannot be discharged after the kidneys, and the blood pressure is increased.
Combined with the above three arguments, the emergence of three types of peripheral vascular fluid renin values in clinically seen cases of renal vascular hypertension can be clarified as follows.
1. High renin-type hypertension, vasoconstrictive hypertension, can cause such a model in animal experiments, narrowing one side of the renal artery, keeping the other side normal, reducing renal blood supply and kidney after renal artery stenosis The decrease of internal pressure promotes the increase of renin secretion, which leads to the increase of angiotensin and produces hypertension. The contralateral kidney is affected by hypertension, which causes the decrease of renin secretion. The increase of renal renin is more than that of Jianshen renin. When the amount is reduced, the plasma renin value is higher than normal, and high renin-type hypertension is formed, and an anti-renin drug can be used for treatment.
2. Low-renin-type hypertension, ie, blood volume-induced hypertension, this animal model is to narrow one side of the kidney animal and remove the contralateral kidney. Because only the isolated kidney, sodium and water discharge are reduced, sodium retention makes the cells The amount of external fluid, that is, the expansion of blood volume, produces hypertension, the intrarenal pressure is not lower than the original level, and the renin secretion is not increased. Under the condition of increased blood volume, the plasma renin value is correspondingly Below normal, the formation of low-renin-type hypertension, the treatment of anti-renin drugs, and the use of diuretic sodium.
3. Normal renin-type hypertension, that is, mixed hypertension, is common in essential hypertension. The kidneys of this type of lesion have both sodium-discharging disorder and increased renin secretion, that is, blood volume increases on the one hand, and arteriolar contraction on the other hand. Strengthening, both can lead to elevated blood pressure, increased blood pressure and increased blood volume can inhibit the secretion of renin, and finally reach equilibrium, that is, renin and aldosterone secretion are within the normal range, in the treatment needs to be combined Apply diuretic sodium and anti-renin drugs.
(two) pathogenesis
1. Animal experiment research
In 1934, Goldblatt et al. first studied dogs, using clamped bilateral renal artery hypertension, and established a basic model of renal hypertension. The unilateral renal artery was clamped to produce only transient hypertension, in order to establish a high persistence. The blood pressure model was later used to clamp the bilateral renal artery or clamp one side of the renal artery, and the contralateral kidney was removed for experimental study. Edmunds et al believe that sheep and rats have a special susceptibility to the two kidneys and one clip hypertension. In the study of renal vascular hypertension, sheep and rat models are better than dogs and rabbits.
Robertson et al. studied animal studies and divided the pathophysiology of renal artery stenosis into three phases. The first phase was often seen in animal experiments. Blood pressure began to rise several minutes after clamping the renal artery, and circulating renin activity ( PRA) and angiotensin II (Ang II) increased in parallel, due to elevated AngII, PRA, AngII and blood pressure quickly returned to normal after removal of the clamp or resection of the stenotic kidney, if the renal artery was clamped for several days Or a few weeks later, enter the second phase, when the blood pressure continues to rise, but the circulating PRA and AngII are not significantly increased, at least the effect of hypertension and the renin-angiotensin system is partially separated, but AngII It may still be an important pathogenesis. If renal artery stenosis or nephrectomy is relieved, hypertension can be relieved. The renin-angiotensin-aldosterone system activity caused by severe stenosis of the unilateral renal artery is found in a small number of patients and animals. Increased, accompanied by a significant increase in blood pressure, manifested as "hypotheronemia hypertension syndrome", if the second phase gradually progressed to the third phase in a few months or years, the blood pressure of this period continues to rise, but PRA and AngII no longer rises, even if the solution Renal artery stenosis or hypertension after nephrectomy did not change, indicating that its pathogenesis is not related to the renin system, due to long-term hypertension leading to damage to the healthy kidney, on the two kidney one clip and one kidney one clip hypertension model The difference is that the former shows that the PRA begins to rise, the chronic phase does not change significantly, the plasma volume is normal, the sodium can be exchanged normally, and the AngII antagonist is effective in reducing blood pressure, while the antihypertensive effect in the chronic phase is not obvious, and the blood pressure is removed after clamping. Can reduce, sodium excretion decreased, the latter showed normal PRA, increased plasma volume, increased exchangeable sodium, no significant reduction in blood pressure of AngII antagonist, blood pressure can be reduced after removal of the clamp, sodium excretion increased.
Some experimental studies have found that the two kidneys and one clip dog maintained a chronic renal ischemia process for 4 weeks, clamping the renal artery and non-clamped kidney, the Ang II content increased, causing renal hemodynamics and microvascular tension changes, but AngII The mechanism of increase is different. The activity of chymase in the kidney is increased, AngI is increased, but the activity of ACE is unchanged. The trypsin inhibitor chmostatin can inhibit the increase of AngII in the kidney, but no intrarenal is found after using a flat su AngII has changed; on the contrary, in the contralateral kidney, Yipingsu can inhibit AngII, while chmostatin has no such effect, indicating that AngI in the clamped kidney is converted to AngII by the action of chymase, while the activity of ACE in the contralateral kidney is increased. , AngI was converted to AngII under the action of ACE.
2. Hemodynamic changes
Animal experimental research provides a pathophysiological basis for the diagnosis and treatment of human renal vascular hypertension. The blood flow to the stenosis side is reduced, and the increase in PRA is found to be more closely related to the increase in renal blood flow than when the PRA is elevated. When <75ml/min, the renal vein renin ratio (RVRR) increased rapidly, and the affected side renin increased, but its distribution changed, suggesting local compensatory effects. Kumura et al applied to aminopurine and inulin for health. Renal, renal vascular hypertension patients with renal function analysis showed that the effective renal plasma flow (ERPF) on the stenosis side was (98 ± 8) ml / (min · m2), glomerular filtration rate (GFR) was ( 24±2) ml/(min·m2), the arteriolar resistance (RA) was (28500±1900) dyn/(scm5), and the small arterial resistance (RE) was (5800±300)dyn/ (scm5), intraglomerular pressure (PG) was (57±1) mmHg, healthy side ERPF was (195±11) ml/(min·m2), and GFR was (48±2) ml/(min · m2), RA is (10 800 ± 600) dyn / (s · cm5), RE is (5800 ± 300) dyn / (s · cm5), PG is (74 ± 1) mmHg, indicating stenosis ERPF, GFR , PG decreased, but RA increased significantly, and the degree of mean arterial pressure, renal artery stenosis, RA=[(MAP-PG)/ERBF]×1328, the stenotic kidney is protected, but the contralateral RA is unchanged, so systemic hypertension can be directly transmitted to the glomerulus, resulting in glomerular hypertension, which is the stenosis side. Compensatory response to renal ischemia to maintain normal renal function.
3. Clinical research
Unilateral renal artery stenosis (two kidneys and one clip) is renin-dependent hypertension. The balloon catheter can accurately determine the decrease of renal perfusion pressure, Ang II and renal vascular resistance increase, resulting in pressure-diuretic curve displacement, although blood pressure is significantly increased However, the sodium retention is rare, and the blood volume remains unchanged. In the chronic phase, the stenotic kidney continues to secrete renin, and the blood volume and peripheral vascular resistance increase. Therefore, the healthy kidney compensates to strengthen diuretic and sodium, and water is excreted. Plasma volume returned to normal, with ACEI or ARB, blood pressure can be restored to normal or improved after intervention or surgery. When the disease progresses to the third stage, due to long-term hypertension and AngII, the renal arterioles are extensively damaged and the kidneys are small. Spherical sclerosis, even if the stenosis of the kidney can not relieve high blood pressure, bilateral renal artery stenosis and a kidney-clip animal model are somewhat different, not purely volume-dependent hypertension, often manifested as high renin and volumetric hypertension Successively, because bilateral bilateral renal artery stenosis is not a symmetric development, the degree of renal artery involvement and the course of disease are different, so the early manifestation of renin Lai hypertension, the progressive development of capacity-dependent hypertension.
Proteinuria is common in hypertensive patients with renal artery occlusion. Proteinuria excretion is not associated with hypertension, but positively correlated with renal artery occlusion and contralateral renal compensatory increase, reflecting increased concentrations of PRA and AngII, using ACEI or ARB. The post-urinary protein can be reduced.
4. Adjustment factors
In unilateral renovascular hypertension, atrial peptide, bradykinin, prostaglandin (PG), and nitric oxide levels are elevated to counteract the effects of the activated renin-angiotensin system, which is pathophysiological Compensatory mechanism, in the stenotic kidney, both PGI2 and PGE2 are synthesized in the kidney and stimulate the increase of PRA, but the increase of PGI2 and PGE2 is related to the degree of renal artery stenosis, light-moderate renal artery stenosis, renal vein and aorta In plasma, 6-keto-I2 did not change, but PGE and PRA increased compared with healthy kidney, and venous blood was higher than arterial blood. Aspirin inhibited PGE2 synthesis, inhibited PRA release and decreased hypertension, and severe stenosis. -keto-PGF12 and PGE2 are more abundant in the healthy side of the kidney, which seems to promote the release of PRA, and PGI2 is also increased, further enhancing and participating in the release of PRA. Nitric oxide causes relaxation of smooth muscle cells, which has important regulation of renal hemodynamics and vascular dynamics. The role of nitric oxide synthase is inhibited, resulting in increased vascular tone and renal dysfunction.
Prevention
Renal vascular hypertension prevention
The key to prevention is to vigorously prevent and actively treat the primary diseases that cause renal vascular hypertension, such as multiple arteritis and atherosclerosis.
Patients with renal vascular hypertension should take measures against the right medicine, and should be actively treated for a limited time. It is recommended to use traditional Chinese medicine treatment. On the one hand, it can relieve vascular obstruction and restore blood flow to the kidney; on the other hand, it should fundamentally repair and receive The damaged kidney tissue restores normal renal function and the effect is good.
Complication
Renal vascular hypertension complications Complications, hemorrhagic disease, hemophilia, myocardial infarction, heart failure
Renal vascular hypertension with the improvement of diagnostic methods, the continuous improvement of surgical techniques, the improvement of vascular substitute materials, the operative complications are gradually reduced, but due to the differences in medical conditions and doctors' technical proficiency, some complications Occasionally, common complications are as follows.
1, bleeding
Postoperative bleeding is mainly caused by surgical operation. For example, the technique of suturing the blood vessels is poor, the vascular seam is not well matched, the needle spacing is too large, the knotting is not firm, the ligature is loose or the artificial vascular mesh is oozing. .
Precautions: The operator must operate carefully and do not slip. For suturing blood vessels with nylon thread or polyester thread, it is best to use 4 to 5 knots to prevent the ligature from slipping. The vascular seams should be aligned and the spacing should be even. Anti-leakage, suture needles should not be too thick, for dry needle eye bleeding, can be pressed with warm saline gauze for a while; do not rush to suture the bleeding, in order to prevent: "out of the seam, sew out, more and more out of the wolverine situation,
For the application of artificial blood vessels, if the vascular network is larger, there will be more oozing. Therefore, when selecting a blood vessel, it should be a small blood vessel with the same pores.
2, diffuse oozing
This is mainly due to poor blood coagulation, which can be caused by congenital or acquired diseases.
1) hereditary bleeding disorders
Like hemophilia and hereditary fibrinogen deficiency, hemophilia is a tendency of bleeding after traumatic wounds, and the clotting time is prolonged. Most of these patients have a history of bleeding from childhood, and they can get detailed information through preoperative examination. Repeated gum bleeding, nosebleed, menorrhagia, traumatic local skin and mucous membrane bleeding, tooth extraction bleeding, excessive medical history, relatives of several generations of male bleeding abnormalities, should consider the possibility of hemophilia.
2), acquired acquired coagulation dysfunction, may be caused by the following reasons
1 liver function beads and vitamin K deficiency: such as diffuse hemorrhage after water, the general cause is difficult to explain, lead A blood for blood coagulation function check, such as liver dysfunction, partial thromboplastin generation time may occur; if there is liver disease or Vitamin K deficiency, prolonged thrombin time.
2 large amount of blood transfusion: renal revascularization surgery, generally do not require a large number of blood transfusions, once needed, because the number of platelets in the blood of the library is greatly reduced, the function of platelets may also have obstacles, and the V and W factors in the blood plasma are stored. The activity is also greatly reduced, plus the free calcium to reduce the small H value is low, cold temperature and other factors, a large amount of blood can cause diffuse permeation after the blood, and one thinks that the blood of the transport does not exceed 5000ml, if more than this amount, You should lose some fresh blood, reduce the input of dextran, anti-histamine drugs, etc. that affect platelet aggregation.
In the case of diffuse oozing caused by a large amount of blood transfusion, treatment can transport platelets or fresh blood, thus correcting platelet function; and supplementing certain coagulation factors to stop bleeding.
3, plug formation
In renal vascular hypertension, renal revascularization surgery, whether it is internal femoral stripping or bypass surgery, intraoperative, wood can form thrombus on the surface of each anastomosis or around the graft, which is the kidney Common complications of revascularization.
4. Renal failure after renal recanalization
After renal revascularization, renal failure is rare, but for patients with complicated renal reconstruction with hypertension during surgery or preoperative renal disease, renal dysfunction is Very common, in most patients, during the reconstruction surgery, the collateral circulation of the kidney is not destroyed, generally ensuring adequate blood perfusion of the kidney, clamping the main artery of the kidney for 60-90 minutes and rarely occurring renal function. Significant decline, if the collateral circulation is damaged during surgery or systemic hypotension has occurred, renal perfusion may only reach the marginal cortex, and damage to the renal tubule will be difficult to avoid.
Patients with renal vascular hypertension should pay special attention to water and electrolyte balance before surgery. Many of these patients often limit the intake of water due to the results of drug treatment. Some people advocate that when the renal artery is obstructed, preoperative, surgery After appropriate water supply, mannitol and diuretics are necessary, because these measures can temporarily maintain the production of urine, otherwise severe hypoperfusion will occur, it is difficult to prevent kidney damage.
5, heart failure, myocardial infarction.
Symptom
Renal vascular hypertension symptoms common symptoms systolic murmur secondary hypertension twitching abdominal vascular murmur dizziness proteinuria
1. High blood pressure: high blood pressure in young people, sudden high blood pressure in the elderly, often accompanied by severe headache, dizziness, nausea, vomiting, blurred vision and other symptoms. In severe cases, convulsions may occur, even coma, generally Antihypertensive drug treatment is ineffective, hypertension is characterized by rapid development, short course of disease, mostly persistent, and diastolic blood pressure is significantly increased, generally > 15.96: kPa (120 mmHg).
2. Abdominal vascular murmur: Two-thirds of patients can hear systolic murmurs or mild tremors in the upper abdomen or back.
3. There may be intermittent claudication, low back pain, hip pain and other low blood supply to the lower extremities.
4. When the renal artery is embolized, there may be abdominal pain, fever, and elevated blood levels.
5. Hematuria and proteinuria may occur in patients with impaired renal function.
6. Fundus changes show the fundus manifestations of hypertension.
Examine
Renal vascular hypertension check
Laboratory inspection
1. Peripheral plasma renin activity (PRA) determination
According to Rudnick et al., 24 reports showed that the sensitivity of peripheral blood PRA to the diagnosis of renal vascular hypertension was 57%, and the specificity was 66%. Muller et al. proposed a PRA challenge test. After taking captopril 50 mg, the PRA increased significantly after 1 h:
1PRA12ng/(ml·h);
2 PRA absolute value increase 10ng / (ml · h);
3PRA increased 150/100, its diagnostic sensitivity was 74%, specificity was 89%. Because of the higher false positives diagnosed by this method, especially those with higher basal PRA levels, it is more prone to false positives. Not used.
2. The ratio of renal vein renin activity (RVRR)
Normally, renal vein PRA increased by 25% compared with renal artery. If the renal venous blood PRA increased by more than 50% compared with the healthy side, it can be diagnosed as renal artery stenosis. Most scholars believe that RVRR>1.5, healthy renal vein and The distal inferior vena cava PRA is characterized by unilateral renal artery stenosis. Because the renal vein PRA is significantly increased in the affected side, the renin is inhibited by the feedback mechanism, so the PRA is equal to the distal inferior vena cava PRA. However, the actual effect of various factors is not absolutely equal, as long as the ratio of the contralateral renal vein to the distal inferior vena cava PRA (RcCCR) <1.3, (conservative renal vein PRA-inferior vena cava PRA) / inferior vena cava PRA ( Rc-C/C) ratio <0.24, reflecting normal or non-functional stenosis of the healthy renal artery. In unilateral renal artery stenosis, RVRR 1.5 accounted for 77%. The above indicators can predict the success rate of intervention or surgery. Up to 100%, but this method still has 50% false negative. In order to increase the positive rate and reduce the false negative rate, the captopril challenge test is used. Captopril 25~50mg, before taking the drug and 60min after taking the drug, respectively Renal venous blood samples were measured for PRA, and RVRR, renin challenge test and sodium were calculated. The intake is closely related, the Chinese people have more sodium intake, so the renin secretion is inhibited. Our study believes that after taking captopril 25mg for 60min, RVRR>2.5, the diagnosis is positive, can make RVRR more than before the challenge The positive rate of diagnosis increased by 14%. Rossi et al. concluded that RVRR is more diagnostic for nephrectomy in patients with renal artery occlusion with renal atrophy. In patients with bilateral renal artery stenosis, only the renal artery occlusion side PRA Increased, with differential diagnosis.
Film degree exam
Radionuclide examination
Captopril interventional renal dynamic imaging is a non-invasive method for the diagnosis of renal vascular hypertension. The sensitivity and specificity of this method are different from each report, which may be related to case-like, pre-inspection preparation and technical conditions. The sensitivity of diagnosis is 62%99%, and the specificity is 91%98%. Among them, the sensitivity difference is large, which reflects more false negatives. The two groups of captopril and captopril plus furosemide are examined. There was no significant difference in sensitivity and specificity.
Positive criteria for captopril test renal imaging: 1 kidney volume reduction; 220min clearance rate decreased by >10%; 3 peak ratio decreased by >10%; 4 peak extended by more than 2min; 5 renal blood perfusion time prolonged, in line with the above Three of the five items were diagnosed as positive, but there are still some false positives and false negatives in this method. The clinical combination should be combined with the patient's condition and antihypertensive effect.
(1) False positive:
1 calcium channel blockers can interfere with captopril renal imaging, causing dilatation of the small arteries, decreased perfusion pressure, resulting in decreased glomerular filtration rate, manifested as bilateral symmetric renal dysfunction, so before the test Calcium channel blockers should be discontinued.
2 hyponatremia or low-salt diet, can activate the renin-angiotensin system.
3 After taking captopril, hypotensive reaction occurred, and the mean arterial pressure decreased by >20 mmHg, which led to a decrease in renal perfusion pressure and glomerular filtration rate, and bilateral bilateral symmetric radioactivity distribution was abnormal.
4 The injection of radiopharmaceuticals flows into the skin, causing the drug to be taken into the blood by the kidney without a significant renal curve, and the performance continues to rise.
(2) False negative:
1 atherosclerotic renal vascular hypertension, PRA may be normal, prone to false negative.
2 Gastrointestinal diseases: affecting the absorption of captopril, 60 minutes after the service, the drug concentration has not reached the peak.
3 long-term use of ACEI or ARB drugs, affecting the sensitivity of captopril, so the above drugs were discontinued 48 hours before the examination.
4 check the advance food, affecting drug absorption.
5 bilateral renal artery severe stenosis with collateral circulation.
6 bilateral renal artery severe stenosis or renal insufficiency, the sensitivity and accuracy of imaging is low.
7FMD is limited to the local stenosis of the middle segment and branch of the renal artery, and the false negative rate can reach 50%.
Losartan (Chosya), an angiotensin II receptor blocker, is easily absorbed by oral administration and is not affected by food. However, it can not be examined 4 hours after the drug is taken. It is not suitable for routine clinical application and is highly suspected only in clinical practice. The disease, and the captopril test negative, can improve the sensitivity of the diagnosis, aspirin interventional renal imaging, can significantly improve the sensitivity of the diagnosis, but this method has not been widely used in the clinic.
2. Ultrasound examination
A non-invasive method for the diagnosis of renal artery stenosis for clinical application, the success rate of the examination is 80% to 90%, 10% to 20% due to the technical level of examination, the patient is obese, the abdominal gas is high, the renal artery is short, and the examination is not possible. Successfully, the sensitivity and specificity of this method are high. The diagnosis of renal artery stenosis, the efficacy and follow-up review after interventional therapy are very valuable. The waveform of normal main renal artery is impedance-type continuous forward diastolic blood. The flow rate (PSV) is 60-120 cm/s, and the resistance index (RI) is the degree of measurement of intra-renal artery impedance. The calculation formula is [1-(end-diastolic velocity/maximal contraction velocity)]×100, The normal value is 58 to 64. If the adult is more than 75 abnormalities, ultrasound Doppler diagnosis of renal artery proximal stenosis has a hemodynamic significance. PSV is the most important diagnostic indicator. If PSV>180cm/s, reflect the kidney. Arterial stenosis >60%, PSV>220cm/s, suggesting stenosis >75%, renal artery flow rate / abdominal aorta flow rate ratio (RAR) is an indicator to prevent individual flow velocity variability, under normal conditions, RAR<3.5, Hoffman Comparison of ultrasound Doppler and angiography Analysis found to 180cm / s as the critical value, the sensitivity of diagnostic ultrasound of 95%, specificity of 90%.
3. Magnetic resonance angiography (MRI)
This method uses gadolinium to enhance magnetic resonance angiography, which has great value in the diagnosis of renal artery stenosis. Its sensitivity and specificity are more than 90%. There is no special contraindication. The main disadvantage is that the examination cost is high and it is difficult. Routine application; can be artificially false positive, the degree of arterial stenosis is more serious than the actual display, analysis and breathing, bowel movements, renal artery bending, the distal end, intrarenal artery stenosis or para-renal artery stenosis is unclear, Difficult to diagnose, but valuable for the diagnosis of localized stenosis at the opening, especially for some patients with atherosclerotic stenosis, limited to the lesion at the opening, no abnormalities found in angiography, because the right renal artery opening is located behind the abdominal aorta Lateral and stenosis were concealed by abdominal aorta angiography. The hemodynamic examination confirmed that the systolic pressure difference was 80 mmHg. MRA also non-invasively measured renal plasma flow (RPF) and glomerular filtration rate (GFR). To determine the functional significance of renal artery stenosis, for those who install an internal pacemaker or a defibrillator in the body, this method should not be used.
4.CTA check
Spiral CT angiography for renal vascular disease with normal renal function, sensitivity of 98%, specificity of 94%, accuracy is very good, this method compared with angiography (DSA) analysis, renal artery stenosis 50% And the secondary renal artery (96%) developed clearly, CTA more Doppler ultrasound diagnosis is more accurate, if accompanied by renal insufficiency (creatinine > 1.7mg / ml), its diagnostic sensitivity is 93%, specificity 81% Because the contrast dose needs 100ml, it is toxic to the kidney, so the clinical application is limited. This method is only used when the MRA is contraindicated and the kidney function is normal.
5. Angiography
It is still considered to be the "gold standard" for the diagnosis of renal artery stenosis. Clinically commonly used digital subtraction angiography (DSA), the location, extent, extent of renal artery stenosis, distal branch, collateral circulation and renal atrophy are observed. Or surgical treatment provides a reliable diagnosis, more than 20% expansion after stenosis, reflecting severe stenosis, more causes of renal vascular hypertension, especially aortic inflammation is more common, so DSA examination should include the brachiocephalic artery, chest and abdomen Aorta, renal artery, radial artery, femoral artery and pulmonary artery, because of the risk of nephrotoxicity caused by contrast agents, it is recommended to use carbon dioxide or gadolinium.
Diagnosis
Diagnosis and diagnosis of renal vascular hypertension
diagnosis
Diagnosis can be based on medical history, clinical symptoms, and laboratory findings .
Differential diagnosis
1. Post-traumatic renal stenosis: imaging changes are similar to renovascular hypertension, which can also be manifested as hypertension, the kidney volume of the affected side is reduced, but the patient has a clear history of trauma and obvious perirenal hematoma formation, with The hematoma gradually absorbs, mechanizes, and causes pressure on the renal artery. Therefore, the patient's blood pressure is gradually increased, and the renal development of the IVU affected side is delayed, and even severe cases are not developed.
2. Chronic pyelonephritis: also manifested as hypertension and kidney volume reduction, but a history of urinary tract infection; urine routine examination can be found red, white blood cells and protein, cast, IVU kidney volume is reduced, renal function appears in the late stage of the disease When it is not complete, obvious edema can occur.
3. Pheochromocytoma: Hypertension as the main symptom, mostly manifested as paroxysmal hypertension, the systolic blood pressure can reach 26.6kPa (200mmHg), the patient may have pale, palpitation, sweating and other symptoms, benzylamine The oxazoline inhibition test and histamine challenge test were positive. The content of urinary catecholamine and vanillyl mandelic acid (VMA) was high in 24 hours. B-ultrasound and CT examination showed images of adrenal tumors on the affected side.
4. Renal artery embolization: acute phase can be manifested as hypertension, the patient has sudden lumbar pain and hematuria, the kidney of the IVU is not developed, renal angiography shows renal artery interruption and filling defect of intra-arterial thrombus.
5. Occupational lesions at the renal hilum: If the renal artery is compressed, high blood pressure can also occur, but intravenous urography, ultrasonography, CT, MRI scan can be seen in the renal hilum.
6. Kidney drooping: If the sagging kidney can pull the kidney pedicle, it can cause high blood pressure, but there are often symptoms of low back pain and digestive tract dysfunction. Hematuria is also common. After taking the supine position, the symptoms can be alleviated or disappeared. The position of the kidney was significantly changed in the urinary tract angiography or ultrasound examination.
7. Primary aldosteronism: also shows symptoms of hypertension, but moderately elevated blood pressure, a chronic process, poor treatment with antihypertensive drugs; more urinary symptoms, especially at night; symmetry of limbs Muscle weakness or paralysis; hypokalemia and hypokale alkalosis; plasma renin activity decreased; radionuclide adrenal scanning can be seen in a round tumor image, ultrasound, CT, MRI can be found in adrenal tumor imaging.
8. Renal aneurysm: also showed hypertension, but the urinary tract plain film showed circular calcification at the renal hilum; renal angiography showed limited cystic or fusiform expansion of the renal artery.
9. Renal arteriovenous fistula: There are severe hypertension, but there is a history of renal injury; the upper abdomen and the kidney area smell rough and continuous vascular murmur, the venous urography is not developed; the renal angiography shows the pupil close to the heart The lateral renal artery is thickened, its branches are not developed, and the renal vein and inferior vena cava are developed early.
10. Essential hypertension: Although persistent hypertension is also present, intravenous urography is rapid in developing renal pelvis, and the length of the long axis of the two kidneys is not significantly different or less than 1 cm; the radionuclide kidney segment and the secretory segment are reduced. Not obvious.
11. Congenital renal hypoplasia: manifested hypertension and kidney shrinkage, but abdominal auscultation without vascular murmur; intravenous urography is not developed or slow development of the kidney, kidney shadow is small and light, narrow renal pelvis, kidney deficiency For example, the small sputum is short and thick, and the ureter is slender.
