There is one renal artery on the left and right side of the normal kidney, but there are more variants of the renal artery, most commonly the paranephric artery, which originates from the abdominal aorta or branches of the abdominal aorta, mostly directly from the upper or lower pole of the kidney into the kidney, with the former being the majority” J. So far. The study of renal artery variation is mainly cadaveric dissection, and the purpose of the study is also limited to guiding renal transplantation, renal tumor resection and other retroperitoneal surgery, and there are few reports on the relationship between renal artery anatomical variation and hypertension in China. We studied the possibility of renal artery variation causing renal vascular hypertension from June 2002 to February 2 (106) and report as follows. 1. Clinical data (1) General data 11 patients with hypertension, including 9 males and 2 females; age 26-78 years; duration of disease 3 months to 20 years; 8 cases with sudden onset, persistent hypertension [(1611-240)/(100-141))mHg)], 3 The cases had hypertension, but in the past 2 years, they suddenly had difficulty in controlling multiple antihypertensive drugs, and angiotensin-converting enzyme inhibitors (ACEI), angiotensin II receptor antagonists (ARB), and diuretics were ineffective. Physical examination: no abnormalities in cardiopulmonary auscultation, no percussion pain in both kidney areas, peribulbar vascular murmur in 3 cases; normal blood routine; no microscopic hematuria, proteinuria and tubular pattern in urine routine; normal thyroid function, plasma protein, blood glucose and lipids; mild increase in blood urea nitrogen (BUN) and creatinine (cr) and hypokalemia in 4 cases. (2) Peripheral blood renin in prone position (I.41-4.85) n∥ (1nl/h) (normal reference value range 0.05-0.79), standing position (3.67-8.64) .g/(ml/h) (normal reference value range 0.93-6.56). -6.56). Angiotensin II: prone (97.42-216.10) pg/blood (normal reference range 28.20 – 52.20), standing (150.20 – 589.70) pg/ml (normal reference range 55.30 – 115.30). Aldosterone: normal in the standing position in 4 cases, mildly increased in 7 cases, and no change in the standing position. (3) Ultrasound examination showed that both kidneys were normal in shape and size, without stones and occupancy, with no atrophy of the cortex, clear boundary of the cortex and medulla, no separation of the collecting system, and no dilatation of the ureter. The color multispectral showed no clear stenosis of the main trunk of both renal arteries, normal blood flow waveform and normal resistance index. (4) “4Tc-DTPA nephrogram showed a significant decrease in peak unilateral blood flow in 11 cases (7 on the right and 4 on the left) and delayed excretion in 4 cases, including 1 case of localized tracer retention in the kidney, combined with a mild decrease in peak contralateral blood flow and delayed excretion in 4 cases (2 on the right and 2 on the left), a mild decrease in glomerular filtration rate bilaterally in 1 case and unilaterally in 2 cases, and the rest were normal. 8 cases of 16-slice spiral CT (plain+enhanced) showed that the renal arteries were not clearly stenosed. The original images of all renal arteries obtained, combined with multiplanar reconstruction, maximum density projection and volume, showed no occlusion, thrombosis or stenosis of the main renal artery, 2 cases of bilateral collateral renal arteries and 6 cases of unilateral collateral renal arteries (4 on the right and 2 on the left), all emanating from the abdominal aorta. One of them started from above the opening of the left common iliac artery, and each of them traveled independently, entering the renal parenchyma alone and then branching. In the other 3 cases, renal arteriograms showed no stenosis or occlusion of the renal artery opening, main trunk and segmental arteries, and all found the collateral renal arteries (right 1 and left 2) without stenosis or occlusion. 2 cases of selective collateral renal arteriograms showed no stenosis in the anterior part of the kidney and slender branches in the posterior part of the kidney, with clear boundaries of the local kidney supplied by the blood, but delayed emptying of the contrast medium. Selective angiography was abandoned due to difficulties in finding the opening. In the other case, the attempted selective angiography was abandoned due to difficulty in finding the opening. (5) Diagnostic analysis and therapeutic regression There was no family history of hypertension in this group of cases, and the increase in diastolic blood pressure was predominant. Laboratory tests showed hyperrenin, hyperangiotensin and some mild hyperaldosteronism. The isotope renogram showed significant difference in peak renal perfusion between the two sides and a significant unilateral decrease, with mild or normal impaired glomerular filtration. Ultrasonography and CT scan excluded adrenal, renal parenchymal and post-renal obstructive disease, which tended to be renal vascular hypertension. However, further CT and digital subtraction angiography (DSA) examination of the renal artery trunk and major branches showed no stenosis or occlusion, and the renal collateral renal arteries on the side of the blood flow obstruction seen on isotope renogram were found to be variant, mostly slender and tortuous. Clinical diagnosis: renal artery variation (paranephric artery), renal vascular hypertension. The oral ACEI, ARB and diuretic drugs were stopped, and calcium antagonists combined with a and/or B-blockers were used instead, which were effective in lowering blood pressure. 2, Discussion Renal hypertension is closely related to renal artery stenosis, among which the stenosis of the collateral renal artery cannot be ignored. According to the national physical survey data, the three-branch type of renal artery accounts for l_48%, four-branch type 0.11%, and five-branch type 0.04%. “1. Lawrence Ouyang “o summarizes that the discovery rate of paranephric arteries varies in anatomical and renal arteriography results, about 3%-30% of the branches of renal segmental arteries are terminal arteries, which do not coincide with each other in the renal parenchyma. The clinical significance of multiple renal arteries is that they can supply up to 20%-25% of the renal parenchyma, and once one of them becomes diseased, the blood supply to the corresponding renal parenchyma will be endangered, causing the corresponding clinical symptoms. Professor Lei-Shi Lai believes that the lack of characteristic clinical manifestations of renal vascular hypertension poses certain difficulties in diagnosis, and the diagnosis of renal vascular hypertension must be combined with clinical and laboratory tests, especially imaging. Screening tests: ① plasma renin activity measurement can be used for coarse screening of renal vascular hypertension; ② the main features of a positive isotope renogram are reduced nuclein uptake in the diseased kidney, a lower peak than the contralateral side, prolonged peak time, delayed excretion, and the presence of differences in renal blood flow that cannot be explained by hypertension” J. Multiple renal arteries are actually the starting point, stroke, and human kidney site variation of renal segment arteries in renal transplantation , nephrectomy, perirenal surgery, and other clinical workups have important reference value. “1 In this paper, the clinical presentation, plasma renin-angiotensin-aldosterone system (RAAS) measurement, and isotope renogram of the patient were inclined to renal vascular hypertension, but further imaging did not reveal renal artery stenosis lesions, but single or multiple collateral renal arteries were found. It is possible that the slender, tortuous course of the paranephric artery reduces the local renal blood flow and renal perfusion pressure, activates the renin-angiotensin-aldosterone system, inhibits the normal antihypertensive function of the kidney, and leads to hypertension; ACEI, ARB, and diuretic drugs are ineffective, and the local renal function deteriorates due to the dilatation of the glomerular outlet artery in the area supplied by the paranephric artery and the decrease in glomerular pressure, and it has been reported that this The deterioration of renal function is irreversible. For the long-term consideration of protecting normal renal function, patients with clinically suspected renal vascular hypertension should avoid ACEI, ARB, diuretic-type antihypertensive drugs, and calcium antagonists are effective o”. The finding of paranephric artery in this paper is only a relatively reasonable explanation for renal vascular hypertension in our clinical work, and the number of cases is small, and its exact pathogenesis, its status in clinical hypertension, and its long-term effects on renal function need further study.