Regional decreases in renal oxygenation during graded acute renal arterial stenosis: a case for renal ischemia

Ischemic nephropathy describes progressive renal failure, defined by significantly reduced glomerular filtration rate, and may be due to renal artery stenosis (RAS), a narrowing of the renal artery. It is unclear whether ischemia is present during RAS since a decrease in renal blood flow (RBF), O(2) delivery, and O(2) consumption occurs. The present study tests the hypothesis that despite proportional changes in whole kidney O(2) delivery and consumption, acute progressive RAS leads to decreases in regional renal tissue O(2). Unilateral acute RAS was induced in eight pigs with an extravascular cuff. RBF was measured with an ultrasound flow probe. Cortical and medullary tissue oxygen (P(t(O(2)))) of the stenotic kidney was measured continuously with sensors during baseline, three sequentially graded decreases in RBF, and recovery. O(2) consumption decreased proportionally to O(2) delivery during the graded stenosis (19 +/- 10.8, 48.2 +/- 9.1, 58.9 +/- 4.7 vs. 15.1 +/- 5, 35.4 +/- 3.5, 57 +/- 2.3%, respectively) while arterial venous O(2) differences were unchanged. Acute RAS produced a sharp reduction in O(2) efficiency for sodium reabsorption (P < 0.01). Cortical (P(t(O(2)))) decreases are exceeded by medullary decreases during stenosis (34.8 +/- 1.3%). Decreases in tissue oxygenation, more pronounced in the medulla than the cortex, occur despite proportional reductions in O(2) delivery and consumption. This demonstrates for the first time that hypoxia is present in the early stages of RAS and suggests a role for hypoxia in the pathophysiology of this disease. Furthermore, the notion that arteriovenous shunting and increased stoichiometric energy requirements are potential contributors toward ensuing hypoxia with graded and progressive acute RAS cannot be excluded.     

Addition of endothelial progenitor cells to renal revascularization restores medullary tubular oxygen consumption in swine renal artery stenosis

Renal artery stenosis (RAS) promotes microvascular rarefaction and fibrogenesis, which may eventuate in irreversible kidney injury. We have shown that percutaneous transluminal renal angioplasty (PTRA) or endothelial progenitor cells (EPC) improve renal cortical hemodynamics and function in the poststenotic kidney. The renal medulla is particularly sensitive to hypoxia, yet little is known about reversibility of medullary injury on restoration of renal blood flow. This study was designed to test the hypothesis that PTRA, with or without adjunct EPC delivery to the stenotic kidney, may improve medullary remodeling and tubular function. RAS was induced in 21 pigs using implantation of irritant coils, while another group served as normal controls (n = 7 each). Two RAS groups were then treated 6 wk later with PTRA or both PTRA and EPC. Four weeks later, medullary hemodynamics, microvascular architecture, and oxygen-dependent tubular function of the stenotic kidneys were examined using multidetector computed tomography, microcomputed tomography, and blood oxygenation level-dependent MRI, respectively. Medullary protein expression of vascular endothelial growth factor, endothelial nitric oxide synthase, hypoxia-inducible factor-1α, and NAD(P)H oxidase p47 were determined. All RAS groups showed decreased medullary vascular density and blood flow. However, in RAS+PTRA+EPC animals, EPC were engrafted in tubular structures, oxygen-dependent tubular function was normalized, and fibrosis attenuated, despite elevated expression of hypoxia-inducible factor-1α and sustained downregulation of vascular endothelial growth factor. In conclusion, EPC delivery, in addition to PTRA, restores medullary oxygen-dependent tubular function, despite impaired medullary blood and oxygen supply. These results support further development of cell-based therapy as an adjunct to revascularization of RAS.     

Follow up study of 70 patients with renal artery stenosis treated by percutaneous transluminal dilatation.

Between April 1978 and April 1981, 70 patients with hypertension and renal artery stenosis were treated by percutaneous transluminal arterial dilatation. Selection of the patients was based solely on arteriographic criteria. Arteriography after dilatation showed considerable widening of the stenosed area in all patients. In 65 patients the effect of treatment on the blood pressure was assessed during follow up periods of one to four years. In 14 of these patients the hypertension was cured, in 29 it was improved, and in 22 there was no change. Patients with fibromuscular lesions benefited distinctly more than did those with atheromatous stenosis, only one of the 21 patients with fibromuscular lesions showing no change as compared with 21 of the 44 patients with atheromatous lesions. The only serious complication encountered was microcholesterol emboli, which developed in two patients with severe atheromatous lesions of the aorta. In the atheromatous group age and overall renal function had no influence on the blood pressure response. In the subgroup of patients with a unilateral lesion the renal vein renin ratios and asymmetrical curves obtained by renography had only a very limited predictive value. In experienced hands percutaneous transluminal arterial dilatation is relatively safe, and this study suggests that it should be attempted in all patients with renal artery stenosis. Only in patients with severe atheromatosis of the aorta should the risk associated with the catheterisation be weighed against the 50% or so chance of benefit from the procedure.     

小檗碱对动脉粥样硬化性损伤的保护作用

目的:探讨小檗碱对动脉粥样硬化损伤的保护作用。方法:将56只大鼠,随机分为对照组(C),高脂饮食假手术组(HD),肾动脉狭窄组(RAS),肾动脉狭窄高脂饮食组(HD+RAS)。C及RAS组给予正常饮食,HD及HD+RAS组给予高脂饮食,RAS及HD+RAS组采用固定内径银夹夹左肾动脉。饲养12周,每组处死6只进行检测,剩余除C外每日灌胃小檗碱(150mg/kg),C予以等量生理盐水灌服,持续4周,四周后处死进行相同检测,用药前后结果进行对比评价小檗碱功能。结果:与C相比,HD,RAS,HD+RAS组肌酐显著升高(P<0.05),HD及HD+RAS组胆固醇明显升高(P<0.05),超氧化物歧化酶(SOD)在HD,RAS及HD+RAS组显著降低(P<0.05),丙二醛(MDA)在HD,RAS及HD+RAS组显著增高(P<0.05),血管内皮生长因子VEGF在HC,RAS及HD+RAS组表达量升高。给予小檗碱灌胃处理后,检测指标各组间无统计学差异(P>0.05)。结论:小檗碱对动脉粥样硬化性损伤具有良好的保护作用。     

Renal artery stent implantation in a patient with bilateral renal artery stenoses presenting with flash pulmonary edema

We describe a patient with a clinical presentation of moderate renal dysfunction, recurrent hospitalizations for congestive heart failure, and an episode of abrupt-onset pulmonary edema (flash pulmonary edema). Diagnostic angiography revealed triple-vessel coronary artery disease (CAD) and bilateral severe renal artery stenosis. This patient underwent successful bilateral renal artery stent implantation with marked improvement in his functional class without further recurrence of pulmonary edema.     

Renal Artery Stenosis Predicts Coronary Artery Disease in Patients with Hypertension

In hypertensive patients with indication of renal arteriography to investigate renal artery stenosis (RAS) there are no recommendations regarding when to investigate coronary artery disease (CAD). Moreover, the predictors of CAD in patients with RAS are not clear. We aimed to evaluate the frequency and the determinants of CAD in hypertensive patients referred to renal angiography. Eighty-two consecutive patients with high clinical risk suggesting the presence of RAS systematically underwent renal angiography and coronary angiography during the same procedure. Significant arterial stenosis was defined by an obstruction≥70% to both renal and coronary territories. Significant CAD was present in 32/82 (39%) and significant RAS in 32/82 (39%) patients. Both CAD and RAS were present in 25.6% from the 82 patients. Patients with severe CAD were older (63±12 vs. 56±13 years; p = 0.03) and had more angina (41 vs. 16%; p = 0.013) compared to patients without severe CAD. Significant RAS was associated with an increased frequency of severe CAD compared to patients without significant RAS (66% vs. 22%, respectively; p<0.001). Myocardial scintigraphy showed ischemia in 21.8% of the patients with CAD. Binary logistic regression analysis showed that RAS≥70% was independently associated with CAD≥70% (OR: 11.48; 95% CI 3.2–40.2; p<0.001), even in patients without angina (OR: 13.48; 95%CI 2.6–12.1; p<0.001). Even considering a small number of patients with significant RAS, we conclude that in hypertensive patients referred to renal angiography, RAS≥70% may be a strong predictor of severe CAD, independently of angina, and dual investigation should be considered.     

Splint renal function after captopril in unilateral renal artery stenosis.

The renal extraction ratios of 131I-sodium iodohippurate (131I-Hippuran) and 125I-thalamate were greatly reduced on the affected side by 50 mg captopril in seven out of 14 patients with unilateral renal artery stenosis. With long term captopril 150 mg daily the uptake of 99mTc-diethylenetriaminepenta-acetic acid by the affected kidney, which was determined by scintillation camera renography, became almost zero in these seven patients, indicating severe reduction of the glomerular filtration rate. Function of the affected kidney returned on discontinuing treatment. The reduced extraction of sodium iodohippurate probably reflected a shortened plasma transit time through the kidney due to intrarenal vasodilatation. The reduced extraction of thalamate reflected a low filtration fraction, suggesting that the vasodilatation was, at least in part, at the level of the postglomerular arterioles. Captopril had little effect on the contralateral kidney and on the kidneys of 17 patients with essential hypertension, and serum creatinine concentrations showed minor changes. Radioisotope renography should be performed after beginning captopril treatment in patients with renal artery stenosis. This is also recommended for patients given captopril as a third line drug when renal artery stenosis has not been excluded. Hypertension is these patients is often severe and difficult to control. Renal artery disease is not rare in this difficult group and finding seriously impaired renal function on one side during captopril treatment may be diagnostic.     

Reversal of renal dysfunction by targeted administration of VEGF into the stenotic kidney: a novel potential therapeutic approach

Renal microvascular (MV) damage and loss contribute to the progression of renal injury in renovascular disease (RVD). Whether a targeted intervention in renal microcirculation could reverse renal damage is unknown. We hypothesized that intrarenal vascular endothelial growth factor (VEGF) therapy will reverse renal dysfunction and decrease renal injury in experimental RVD. Unilateral renal artery stenosis (RAS) was induced in 14 pigs, as a surrogate of chronic RVD. Six weeks later, renal blood flow (RBF) and glomerular filtration rate (GFR) were quantified in vivo in the stenotic kidney using multidetector computed tomography (CT). Then, intrarenal rhVEGF-165 or vehicle was randomly administered into the stenotic kidneys (n = 7/group), they were observed for 4 additional wk, in vivo studies were repeated, and then renal MV density was quantified by 3D micro-CT, and expression of angiogenic factors and fibrosis was determined. RBF and GFR, MV density, and renal expression of VEGF and downstream mediators such as p-ERK 1/2, Akt, and eNOS were significantly reduced after 6 and at 10 wk of untreated RAS compared with normal controls. Remarkably, administration of VEGF at 6 wk normalized RBF (from 393.6 ± 50.3 to 607.0 ± 45.33 ml/min, P < 0.05 vs. RAS) and GFR (from 43.4 ± 3.4 to 66.6 ± 10.3 ml/min, P < 0.05 vs. RAS) at 10 wk, accompanied by increased angiogenic signaling, augmented renal MV density, and attenuated renal scarring. This study shows promising therapeutic effects of a targeted renal intervention, using an established clinically relevant large-animal model of chronic RAS. It also implies that disruption of renal MV integrity and function plays a pivotal role in the progression of renal injury in the stenotic kidney. Furthermore, it shows a high level of plasticity of renal microvessels to a single-dose VEGF-targeted intervention after established renal injury, supporting promising renoprotective effects of a novel potential therapeutic intervention to treat chronic RVD.     

超声对早期糖尿病肾病的诊断价值及肾动脉血流阻力指数与血清hs-CRP、VEGF的关系分析

目的:研究彩色多普勒超声对早期糖尿病肾病的诊断价值及肾动脉血流阻力指数与血清超敏C反应蛋白(hs-CRP)、血管内皮生长因子(VEGF)的关系。方法:选取从2017年2月～2018年2月兰州大学第二医院收治的早期糖尿病肾病患者50例记为病变组,另取同期于该院进行体检的健康人员50例记为对照组。分别对两组人员进行彩色多普勒超声检查,比较肾血流参数。采用酶联免疫吸附法检测两组人员血清hs-CRP、VEGF水平,并作指标间的相关性分析。结果:病变组肾主动脉、肾锥体两侧叶间动脉、肾段动脉的收缩期峰值速度、舒张期最低速度较对照组降低,病变组肾主动脉、肾锥体两侧叶间动脉、肾段动脉的阻力指数较对照组升高(均P0.05)。病变组血清hs-CRP、VEGF水平较对照组升高(均P0.05)。经Pearson相关性分析显示:早期糖尿病肾病患者肾主动脉、肾锥体两侧叶间动脉、肾段动脉的血流阻力指数与血清hs-CRP、VEGF均呈正相关关系(均P0.05)。结论:彩色多普勒超声应用于早期糖尿病肾病的诊断价值较高,且肾动脉血流阻力指数与血清hs-CRP、VEGF密切相关,临床工作中通过联合检测血清hs-CRP、VEGF,从而有助于早期糖尿病肾病的诊断。     

小檗碱对动脉粥样硬化性损伤的保护作用

目的：探讨小檗碱对动脉粥样硬化损伤的保护作用。方法：将56只大鼠,随机分为对照组（C）,高脂饮食假手术组（HD）,肾动脉狭窄组（RAS）,肾动脉狭窄高脂饮食组（HD＋RAS）。C及RAS组给予正常饮食,HD及HD＋RAS组给予高脂饮食,RAS及HD＋RAS组采用固定内径银夹夹左肾动脉。饲养12周,每组处死6只进行检测,剩余除C外每日灌胃小檗碱（150mg/kg）,C予以等量生理盐水灌服,持续4周,四周后处死进行相同检测,用药前后结果进行对比评价小檗碱功能。结果：与C相比,HD,RAS,HD＋RAS组肌酐显著升高（P〈0.05）,HD及HD＋RAS组胆固醇明显升高（P〈0.05）,超氧化物歧化酶（SOD）在HD,RAS及HD＋RAS组显著降低（P〈0.05）,丙二醛（MDA）在HD,RAS及HD＋RAS组显著增高（P〈0.05）,血管内皮生长因子VEGF在HC,RAS及HD＋RAS组表达量升高。给予小檗碱灌胃处理后,检测指标各组间无统计学差异（P〉0.05）。结论：小檗碱对动脉粥样硬化性损伤具有良好的保护作用。     

Symptomatic carotid ischaemic events: safest and most cost effective way of selecting patients for angiography,before carotid endarterectomy.

OBJECTIVE: To determine the safest, least costly, and most effective way to select patients with symptomatic carotid ischaemic events for carotid angiography before carotid endarterectomy. DESIGN: Prospective cohort study. SETTING: University departments of clinical neurosciences and clinical neurology. PATIENTS: 485 Patients with carotid territory transient ischaemic attacks of the brain (n = 224) or eye (n = 162) or retinal infarction (n = 99) were referred to a single neurologist between 1976 and 1986. INTERVENTIONS: Clinical examination by auscultation over the precordium, supraclavicular fossae, and neck vessels (all patients). Cerebral angiography of patients suitable for carotid endarterectomy. MAIN OUTCOME MEASURES: Financial cost and number of disabling strokes after angiography. RESULTS: 296 Patients were investigated by cerebral angiography. Ischaemic symptoms had occurred in the distribution of 298 internal carotid arteries (symptomatic) that were imaged, two patients having bilateral symptoms. The presence or absence of a carotid bruit and the maximum percentage diameter stenosis of the origin of the symptomatic internal carotid artery were correlated. The prevalence of mild disease (diameter stenosis greater than or equal to 25%) of the symptomatic internal carotid artery was 57%, and if an ipsilateral carotid bruit was heard the probability of mild stenosis rose to 92%. The prevalence of moderate disease of the symptomatic internal carotid artery (stenosis greater than or equal to 50%) was 39%, and if a bruit was heard the probability doubled to 78%. The prevalence of severe internal carotid disease (stenosis greater than or equal to 75%) was 22%, and if a bruit was heard the probability was more than double, at 49%. The direct cost to both the NHS and the private health sector of investigating patients with symptomatic carotid ischaemia was estimated for several strategies of carotid artery imaging and expressed in terms of financial cost and number of strokes after angiography incurred in detecting all patients with diameter stenosis of the symptomatic internal carotid artery of greater than or equal to 25%, 50%, or 75%. To detect diameter stenosis of the internal carotid artery of greater than or equal to 25% it is most cost effective to proceed directly to cerebral angiography in patients with a carotid bruit over the symptomatic carotid bifurcation and to screen patients without a carotid bruit by duplex carotid ultrasonography; patients in whom duplex ultrasonography discloses stenosis of greater than or equal to 25% are then referred for cerebral angiography. To detect only more severe internal carotid disease (stenosis of greater than or equal to 50%) the same policy applies, unless the local duplex ultrasonographic service is particularly efficient and reliable, when it is probably most cost effective and safer to screen all patients by this method irrespective of the findings on cervical auscultation. To detect stenosis of 75% or greater it is most cost effective to screen all patients with duplex ultrasonography, whether a carotid bruit is present or not, because this approach reduces the number of angiograms required, is the least expensive, and results in the least number of strokes after angiography. CONCLUSIONS: Patients selection for cerebral angiography before carotid endarterectomy needs to be appropriate and cost effective. Sound clinical evaluation and duplex carotid ultrasound are required. The findings of this study should not be applied to other medical centres without first considering possible differences in the prevalence of carotid artery disease, the efficiency and reliability of duplex ultrasonography, the local complication rates of cerebral angiography, and the local costs of the imaging procedures.     

Early superoxide scavenging accelerates renal microvascular rarefaction and damage in the stenotic kidney

Renal artery stenosis (RAS), the main cause of chronic renovascular disease (RVD), is associated with significant oxidative stress. Chronic RVD induces renal injury partly by promoting renal microvascular (MV) damage and blunting MV repair in the stenotic kidney. We tested the hypothesis that superoxide anion plays a pivotal role in MV dysfunction, reduction of MV density, and progression of renal injury in the stenotic kidney. RAS was induced in 14 domestic pigs and observed for 6 wk. Seven RAS pigs were chronically treated with the superoxide dismutase mimetic tempol (RAS+T) to reduce oxidative stress. Single-kidney hemodynamics and function were quantified in vivo using multidetector computer tomography (CT) and renal MV density was quantified ex vivo using micro-CT. Expression of angiogenic, inflammatory, and apoptotic factors was measured in renal tissue, and renal apoptosis and fibrosis were quantified in tissue sections. The degree of RAS and blood pressure were similarly increased in RAS and RAS+T. Renal blood flow (RBF) and glomerular filtration rate (GFR) were reduced in the stenotic kidney (280.1 ± 36.8 and 34.2 ± 3.1 ml/min, P < 0.05 vs. control). RAS+T kidneys showed preserved GFR (58.5 ± 6.3 ml/min, P = not significant vs. control) but a similar decreases in RBF (293.6 ± 85.2 ml/min) and further decreases in MV density compared with RAS. These changes were accompanied by blunted angiogenic signaling and increased apoptosis and fibrosis in the stenotic kidney of RAS+T compared with RAS. The current study shows that tempol administration provided limited protection to the stenotic kidney. Despite preserved GFR, renal perfusion was not improved by tempol, and MV density was further reduced compared with untreated RAS, associated with increased renal apoptosis and fibrosis. These results suggest that a tight balance of the renal redox status is necessary for a normal MV repair response to injury, at least at the early stage of RVD, and raise caution regarding antioxidant strategies in RAS.     

Persistent kidney dysfunction in swine renal artery stenosis correlates with outer cortical microvascular remodeling

Percutaneous transluminal renal stenting (PTRS) does not consistently improve renal function in patients with atherosclerotic renovascular disease, but the mechanisms underlying irreversible kidney injury have not been fully elucidated. We hypothesized that renal dysfunction after PTRS is linked to ongoing renal microvascular (MV) remodeling. Pigs were studied after 10 wk of atherosclerosis and renal artery stenosis (ARAS), ARAS treated with PTRS 4 wk earlier, and normal controls (n = 10 each). Renal blood flow (RBF) and glomerular filtration rate (GFR) were studied using multidetector computer tomography. Renal microvascular architecture (micro-CT), angiogenic activity, oxidative stress, and fibrosis were evaluated ex vivo. Four weeks after PTRS, blood pressure was normalized. However, GFR and RBF remained similarly decreased in untreated ARAS and ARAS+PTRS (P < 0.05 vs. normal). MV rarefaction was unaltered after revascularization, and the spatial density of outer cortical microvessels correlated with residual GFR. Interstitial fibrosis and altered expression of proangiogenic and profibrotic factors persisted after PTRS. Tubulointerstitial injury in ARAS persisted 4 wk after mechanically successful PTRS, and vessel loss correlated with residual renal dysfunction. MV loss and fibrosis in swine ARAS might account for persistent renal dysfunction after PTRS and underscore the need to assess renal parenchymal disease before revascularization.     

Effect of prostaglandin A1 infusion in hypertensive patients with renal artery stenosis

Clinical data, arteriographic findings, peripheral and renal vein plasma renin activity (PRA) studies and responses to prostaglandin A1 infusion are presented from observations in seven hypertensive patients with renal artery stenosis. PGA1 infusion caused an increase in PRA and urine sodium excretion but no significant change in blood pressure. Exaggerated increases in PRA were observed in five patients. With cessation of PGA1 infusion PRA returned toward pre-infusion levels. In two patients bilateral renal and peripheral vein PRA's were determined before and during PGA1 infusion. PGA1 caused a greater increase in renal vein PRA than in peripheral vein PRA indicating a direct enhancement of renin secretion. These studies indicate possible relationships between the vasoactive prostaglandins and the renin-angiotensin system in the pathogenesis of hypertension due to renal artery stenosis.     

Pressor responsiveness in renal prehypertensive rabbits with a denervated kidney

Norepinephrine was infused iv at several doses into four groups of conscious rabbits (six per group), and the pressor responses were recorded. The groups were 3-day sham-operated rabbits; 3-day, two-kidney rabbits with unilateral renal artery stenosis (RAS); 3-day, two-kidney rabbits with unilateral renal denervation; and 3-day, two-kidney rabbits with unilateral renal denervation plus RAS of the denervated kidney. The rabbits with RAS of an innervated kidney and those with RAS of a denervated kidney had the same pressor responses to norepinephrine, which were greater than the pressor responses in the sham-operated rabbits or in the rabbits with a denervated kidney but without RAS. Four additional groups of similarly prepared rabbits were infused with norepinephrine at 800 ng/min/kg body wt, and mean arterial pressure and cardiac output were determined before and during norepinephrine infusion. The rabbits with RAS of an innervated or of a denervated kidney had greater increases in total peripheral resistance as well as in mean arterial pressure during norepinephrine infusion than did the two groups of rabbits without RAS. This indicated that the rabbits with RAS also had increased vascular responses to norepinephrine. The concentration of norepinephrine in six denervated kidneys was extremely low as compared to that of six innervated kidneys. Because renal denervation did not diminish pressor and vascular hyperresponsiveness in 3-day RAS rabbits, the signal that originates in the kidney following RAS and that results ultimately in pressor and vascular hyperresponsiveness is not mediated by renal nerves.     

Flow visualisation study of spiral flow in the aorta–renal bifurcation

The aim of this study was to analyse the flow dynamics in an idealised model of the aorta–renal bifurcation using flow visualisation, with a particular focus on the effect of aorta-to-renal flow ratio and flow spirality. The recirculation length was longest when there was low flow in the renal artery and smaller in the presence of spiral flow. The results also indicate that patients without spiral flow or who have low flow in the renal artery due to the presence of stenosis may be susceptible to heightened development of atherosclerotic lesions.     

Does Lower Limb Exercise Worsen Renal Artery Hemodynamics in Patients with Abdominal Aortic Aneurysm?

Renal artery stenosis (RAS) and renal complications emerge in some patients after endovascular aneurysm repair (EVAR) to treat abdominal aorta aneurysm (AAA). The mechanisms for the causes of these problems are not clear. We hypothesized that for EVAR patients, lower limb exercise could negatively influence the physiology of the renal artery and the renal function, by decreasing the blood flow velocity and changing the hemodynamics in the renal arteries. To evaluate this hypothesis, pre- and post-operative models of the abdominal aorta were reconstructed based on CT images. The hemodynamic environment was numerically simulated under rest and lower limb exercise conditions. The results revealed that in the renal arteries, lower limb exercise decreased the wall shear stress (WSS), increased the oscillatory shear index (OSI) and increased the relative residence time (RRT). EVAR further enhanced these effects. Because these parameters are related to artery stenosis and atherosclerosis, this preliminary study concluded that lower limb exercise may increase the potential risk of inducing renal artery stenosis and renal complications for AAA patients. This finding could help elucidate the mechanism of renal artery stenosis and renal complications after EVAR and warn us to reconsider the management and nursing care of AAA patients.     

Pressor and vascular responsiveness in renal prehypertensive rabbits with a nonfiltering kidney

This study examined the possibility that the renal tubules are the site of the sensors that respond to renal artery stenosis (RAS) and which initiate the events leading to pressor hyperresponsiveness. A nonfiltering kidney (NFK) was produced in 32 rabbits by 2 hr of total renal ischemia plus permanent ligation of the ureter; the opposite kidney remained undisturbed. Sixteen of these rabbits also received RAS of the NFK. An additional 16 rabbits received RAS without production of a NFK, and 16 more rabbits were sham-operated controls. In acute experiments 3 days later in conscious rabbits, infusions of norepinephrine at several doses resulted in greater increases in mean arterial pressure in the RAS rabbits, with filtering kidneys (2-K, 1-clip) and with NFKs (2-K, 1-clip with NFK), than in the NFK rabbits without RAS (2-K control with NFK) or in the control rabbits (2-K control). Measurements of cardiac output revealed greater increases in total peripheral resistance as well as in mean arterial pressure in response to norepinephrine in the RAS rabbits both without and with a NFK. Because production of a NFK in rabbits did not prevent the development of pressor and vascular hyperresponsiveness 3 days after RAS, these studies indicated that the renal sensors that detect changes in the kidney following RAS and which initiate the series of events leading to pressor and vascular hyperresponsiveness, probably are not located in the renal tubules.     

Evaluation of the Urea Washout Pyelogram and Urography in the Assessment of Renovascular Hypertension

The urea washout (UWT) modification of the intravenous pyelogram was used to study 146 hypertensive patients in order to detect the presence of significant renovascular abnormalities. A positive result was obtained in 55 patients and direct confirmation of main renal artery stenoses by selective renal arteriography was obtained in 26. Bilateral abnormalities were confirmed in seven of the 26 patients. No false-negative results were encountered. The usefulness of this test as a comprehensive screening test is outlined. It demonstrated a high degree of accuracy in the diagnosis of significant unilateral or bilateral main renal artery stenosis in addition to the detection of diffuse intrarenal arteriolar disease. It was of value in the postoperative assessment of operative repair of main renal artery defects. The urea washout test embodies both an anatomical and a physiological approach in the roentgen diagnosis of curable renovascular hypertension. The altered physiology resulting from significant main renal artery stenosis makes possible the use of the urea washout intravenous pyelogram. The value of other forms of intravenous pyelography is described.     

Effect of prostaglandin A1 infusion in hypertensive patients with renal artery stenosis

Clinical data, arteriographic findings, peripheral and renal vein plasma renin activity (PRA) studies and responses to prostaglandin A₁ infusion are presented from observations in seven hypertensive patients with renal artery stenosis. PGA₁ infusion caused an increase in PRA and urine sodium excretion but no significant change in blood pressure. Exaggerated increases in PRA were observed in five patients. With cessation of PGA₁ infusion PRA returned toward pre-infusion levels. In two patients bilateral renal and peripheral vein PRA's were determined before and during PGA₁ infusion. PGA₁ caused a greater increase in renal vein PRA than in peripheral vein PRA indicating a direct enhancement of renin secretion. These studies indicate possible relationships between the vasoactive prostaglandins and the renin-angiotensin system in the pathogenesis of hypertension due to renal artery stenosis.