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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied clinical and biological data occurring in 165 patients observed during 23 years and afflicted with polyarteritis nodosa. Hypertension was present in 52 patients (31.5%) and seven of them suffered from malignant hypertension (4%). Mean age of patients (6 male, 1 female), with malignant hypertension was 38 +/- years old. Mean follow up was 49 +/- 28 months including 26 +/- 21 months after discontinuation of treatment of polyarteritis nodosa. Malignant hypertension occurred during the first year of evolution of polyarteritis nodosa. Renal insufficiency was present in 5 of 7 patients. Proteinuria was greater than 1 gr/d in 4 cases. Renal arteriography was performed in 6 patients and showed in every case renal ischemia and microaneurysms in five. In 4 patients measurements of plasma renin activity and of aldosterone were obtained. A stimulation of those hormones was demonstrated. Some symptoms of polyarteritis nodosa were present with a high incidence in case of malignant hypertension: digestive signs (6/7), orchitis (3/6). HBs antigen was present in 6 cases and hepatitis in 5. Captopril was effective in every case, alone or associated with other treatments. Follow up of hypertension went from 8 months to 4 years. At present time 6 patients are alive and one is lost of follow up. A treatment is necessary in 6 of 7 patients. Creatininemia is greater than 300 micromol/l in 4 patients. A successful kidney transplantation was performed in one case. Our study shows a close relation between malignant hypertension observed in polyarteritis nodosa, vascular nephropathy, digestive and urologic signs. Hepatitis B virus could be responsible of those manifestations.
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PMID:[Malignant arterial hypertension in periarteritis nodosa. Incidence, clinicobiologic parameters and prognosis based on a series of 165 cases]. 287 20

The neurohormonal contribution to high blood pressure was investigated in 9 conscious two-kidney, two-clip Goldblatt (2K2C) hypertensive dogs during evolution of the benign and malignant phases after application of bilateral renal clips (BRC). Serial measurements were taken of the plasma renin activity (PRA), plasma angiotensin I-immunoreactivity (Ang I-ir), plasma angiotensin II-ir (Ang II-ir), renin substrate (RS) catecholamines [epinephrine (Epi) and norepinephrine (NE)] and vasopressin (AVP). Immediately after BRC, the elevation of the blood pressure (86 +/- 3 to 110 +/- 3 mmHg, p less than 0.01) was associated with an increase in heart rate (93 +/- 3 to 114 +/- 9 beats/min, p less than 0.01). These hemodynamic changes were accompanied by increases in PRA, Ang I-ir, Ang II-ir, Epi, NE and AVP. The renin angiotensin system was activated throughout the 3 week period following BRC, as indicated by increases in PRA, Ang I-ir and Ang II-ir. Catecholamines were elevated immediately after BRC, followed by a return toward the control values. AVP underwent a slight but not significant elevation after BRC, which was sustained during the 3 weeks. Production of malignant hypertension was affected by occlusion of one of the adjustable renal clips 3 weeks after BRC. A marked elevation of the blood pressure was associated with significant increases in PRA, Ang I-ir, Ang II-ir, Epi, NE and AVP, compared with the pre-occlusion values. In addition, pharmacologic experiments were performed in 6 of 9 dogs. Administration of angiotensin I converting enzyme inhibitor (SQ 14225) reduced the blood pressure both in the benign and malignant phases of 2K2C renovascular hypertension, and a ganglionic blocking agent (hexamethonium) also decreased the blood pressure. However, a specific, vascular acting AVP antagonist failed to reduce the blood pressure significantly. From this study, it seems likely that severe renal ischemia caused by renal clipping caused the activation of the renin-angiotensin and the sympathetic nervous system and elevation of serum vasopressin. However, there are no apparent differences between the benign and malignant phases of renovascular hypertension, except for the marked elevation of neurohormone levels in malignant hypertension.
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PMID:Characterization of neurohormonal changes following the production of the benign and malignant phases of two-kidney, two-clip Goldblatt hypertension. 288 73

Our previous studies support the hypothesis that activation of the renin-angiotensin system by renal ischemia elevates adenosine levels and that adenosine acts in a negative feedback loop to limit renin release and to mitigate some of the hypertension-producing effects of angiotensin II. To further test this hypothesis, we compared the time course of caffeine-induced increases in plasma renin activity with the time course of changes in plasma levels of adenosine in two models of renin-dependent renovascular hypertension. Also, we compared the effects of caffeine on plasma renin activity and arterial blood pressure in renin-dependent versus renin-independent renovascular hypertension. In comparison to sham-operated rats, plasma levels of adenosine in the left and right renal veins and aorta were elevated severalfold in two-kidney, one clip rats (2K1C) 1 week after left renal artery clipping. However, adenosine levels declined during the second and third weeks after clipping. In 2K1C rats treated chronically with caffeine, plasma renin activity was markedly elevated during the first week after operation as compared to non-caffeine-treated 2K1C rats. However, during the second and third weeks after clipping, caffeine had lesser effects on plasma renin activity. A temporal relationship between plasma adenosine levels and caffeine-induced hyperreninemia was also observed in rats with aortic ligation. Caffeine accelerated hypertension in 2K1C rats and rats with aortic ligation (renin-dependent renovascular hypertension), but it had no effect on plasma renin activity or blood pressure in one-kidney, one clip rats (renin-independent renovascular hypertension). These results lend further support to the hypothesis that adenosine functions to mitigate the renin-angiotensin system in renin-dependent renovascular hypertension.
Hypertension 1988 Aug
PMID:Adenosine in renin-dependent renovascular hypertension. 304 93

Baseline and single-dose captopril scintigraphy with 1 mCi of 99mTc-diethylenetriamine-pentaacetic acid (or 99mTc-glucoheptonate) was performed in 5 neonates with renovascular hypertension. Unilateral renal artery thrombosis and/or renal infarction was associated with severe impairment or lack of function on both studies (3 patients). Renal ischemia due to aortic thrombus manifested itself as lack of function only following captopril (2 patients). This approach predicted renal failure as a side effect of captopril therapy in 2 patients, 1 with unilateral (contralateral kidney infarcted) and the other with bilateral renal ischemia from aortic thrombus. Single-dose captopril scintigraphy may be a useful tool to predict tolerance to captopril therapy.
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PMID:Single-dose captopril scintigraphy in the neonate with renovascular hypertension: prediction of renal failure, a side effect of captopril therapy. 306 Jan 99

Renovascular hypertension is the most prevalent form of curable hypertension. Despite some unanswered questions, there is a growing consensus about the need to identify patients with renovascular hypertension so that a specific therapy can be recommended. The renin-angiotensin system is the chief pathophysiologic mechanism responsible for hypertension in patients with renal ischemia but other, yet poorly defined, mechanisms may be operative. Most patients with renovascular hypertension do not present with typical or discriminative clinical features. Thus, many physicians do not perform work-up to uncover renovascular disease even if diagnosis is dictated by patients' clinical course. It is difficult to make the proper diagnosis unless there is a high index of suspicion and certain procedures are performed. How can we, then, select a few patients for the work-up from the vast sea of people with hypertension? The identification of such patients and the pursuit of a renovascular etiology is a matter of clinical judgment. Delineation of renovascular hypertension should be undertaken only after careful deliberation. When clinical clues suggestive of renovascular hypertension are present, appropriate diagnostic tests should be undertaken in patients who are candidates for PTRA or surgery. Captopril-stimulated PRA test is done first. If the test is positive (and in some clinically relevant circumstances even if it is not done or is negative), DSA should be obtained. IV-DSA is being steadily replaced by the superior IA-DSA. The need for renal vein renin determination varies from center to center, but when carefully performed, it yields meaningful information. Ultimately, a conventional arteriogram is done to define the extent of renal artery stenosis and to assess intrarenal vascular anatomy. For selected patients, the benefit-risk ratio clearly outweighs the cost considerations. The spectrum of renovascular hypertension is variable, further compounding the diagnostic indications and contraindications. At one end of this spectrum are those patients in whom surgical therapy is likely to be beneficial, and at the other end are the patients who have relative contraindications to surgery. In between lies the vast gray zone that constitutes a great judgmental challenge in clinical medicine. What is to be done with the patients who have mild to moderate renovascular hypertension whose BP is controlled on medical therapy? There are some patients who may benefit from renovascular repair despite the nonlateralization of renal vein renins. What is the mechanism underlying their hypertension?(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renovascular hypertension. 306 42

Placental ischemia is one of the etiological factors of pregnancy induced hypertension (PIH), however, the pathogenesis of placental and renal ischemia has not been clarified. The purposes of this investigation are (1) to clarify the fetomaternal hemodynamic changes in PIH and the influence of maternal postural change on fetomaternal hemodynamics, measured by thermodilution method, impedance cardiography and pulsed doppler method during pregnancy, (2) to provide to relationship between intrauterine resting tonus and maternal hemodynamics, that is, blood pressure, placental and renal blood flow measured by electromagnetic flowmeter and thermocouple method, and renal nerve activity, and (3) to study the influence of placental ischemia on vascular sensitivity to angiotensin II measured by Magnus method in animal experiment. (1) The increase in C.O and blood volume were recognized from the beginning of pregnancy to 24 GW, and subsequently, the decreasing tendency were found from about 32 GW to the onset of labor. However this decreasing tendency were subsided in the lateral position. These circulatory changes were observed in both normotensive and PIH cases, and especially, the decrease in C.O and blood volume in late pregnancy were more remarkable in PIH than that in normotensive pregnancy. From the results of Starling curve, left ventricular work was more hyperdynamic status in PIH than that in normotensive pregnancy, these results show that there are a compensatory mechanism against high vascular resistance in PIH. A/B (S/D) ratio in uterine artery, umbilical artery and fetal aorta were lowered in II-nd and III-rd trimester and more decreased in the lateral position from the supine position, on the other hand these ratio in PIH were elevated respectively. These results show that there are the aortocaval compression by the heavy tensive uterus and subsequent sluice flow mechanism in fetoplacental circulation in the supine position in late pregnancy. (2) These vascular compression were recognized very often in PIH accompanying with increasing in uterine resting tonus. It was recognized in pregnant rabbit that an increase in uterine resting tonus in the ovarian side caused an increasing blood pressure, a decrease in renal and placental blood flow and an increase in renal sympathetic nerve activity (RSNA). After resection of the suspensory ligament of ovarii, an increase in resting tonus in the ovarian side did not only cause an increase in RSNA, but also a decrease in renal blood flow.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinical and experimental studies on the pathogenesis in pregnancy induced hypertension]. 325 61

In coarctation, bipedal exercise induces a pressure triad: exaggerated systolic arm hypertension, unchanging leg pressure, and markedly increased systolic gradient. Constancy of leg pressure derives from the lower body sharing the poststenotic compartment with the kidneys. Exercise-induced poststenotic hypotension stimulates the juxtaglomerular apparatus (JGA) to raise renal pressure to pre-exercise levels. Ambulation during the greater part of each day stimulates the JGA repetitively. Thereby, this chronic Single-Kidney-Goldblatt model is modified by increased plasma renin, fluid volumes, and cardiac output. It also accounts for hyper-responsive renin output after renin blockage and for mild poststenotic hypertension. Hypertension after repair which corrected the resting gradient, is almost always associated with the exercise triad, indicating that renal ischemia exists during ambulation. Thus, residual hypertension usually means residual coarctation. Mesenteric ischemia complicating postoperative paradoxic hypertension is probably due to spasm in the superior mesenteric artery and not to fixed occlusion of necrotizing arteritis.
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PMID:Coarctation hypertension is renovascular, modified by ambulation. Coarctation hypertension renovascular variant. 352 15

Renal parenchyma, and the juxtaglomerular apparatus in particular, was studied in 23 patients with verified diagnosis of pheochromocytoma. Intraoperative renal biopsy was performed in 21 cases, and kidneys obtained at nephrectomy or autopsy were examined in 2 cases. Twenty-one patients were examined following the removal of pheochromocytoma (2 patients died). Arterial BP returned to normal in 86.4%, and residual hypertension due to continuous hyperfunction of the juxtaglomerular apparatus in the presence of hypertensive angiosclerosis was recorded in 13.6%. Tubular epithelial atrophy of varying markedness, associated with renal ischemia, was detected in all cases. The pathogenetic contribution of the renin-angiotensin system to pre- and postoperative hypertension in pheochromocytoma patients is discussed.
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PMID:[Residual hypertension after removal of a pheochromocytoma (morphologic study of the kidneys)]. 368 71

Symptomatic juxtarenal aortic atherosclerosis is a rare and threatening form of aortic disease. The formidable implications of complex aortic reconstruction, the high operative mortality and morbidity rate and the uncertainties regarding the beneficial effects of operation combined to foster highly conservative attitude regarding management. Our reported experience and a brief review which has been highlighted in this report, support an aggressive use of combined aortic and renal branch repair rather than a staged repair or medical management. Operative mortality was higher only in the patients with the most extensive patterns of atherosclerosis. This should caution careful preoperative assessment in order to plan optimum technique and extent of the reconstruction for these higher risk patients. The renal revascularization had a significant beneficial effect on hypertension and excretory function observed both early and late following operation. Furthermore a lower than expected late mortality supports our contention that combined aortic and renal reconstruction increases survival of the patients by preventing the complications of progressive renal ischemia, accelerated hypertension, and renal failure.
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PMID:Operative treatment of juxtarenal aortic atherosclerosis. 386 7

Vesicoureteral reflux (VUR) is mainly a primary phenomenon due to incompetence of the ureterovesical junction, mostly affecting a pediatric population. During micturition cystourethrography (MCU) reflux into the kidney--intrarenal reflux (IRR)--is occasionally seen. In areas with IRR the kidney surface may subsequently be depressed and the papillae retracted (reflux nephropathy (RN]. VUR may lead to hypertension and/or end-stage renal failure. Most commonly, VUR is discovered during evaluation for urinary tract infection, but it may also be present in patients with hypertension, toxemia of pregnancy, chronic renal failure and proteinuria, and it may be found in siblings of patients with VUR. For the time being VUR is demonstrated at radiographic MCU, whereas RN is diagnosed by demonstration of focal scars and of abnormal parenchymal thickness at urography. In children with VUR and no abnormalities of calyces or parenchymal defects standardized measurement of the parenchymal thickness at three sites may identify kidneys which are likely to develop focal scars. Quantitation of focal scarring should be performed in connection with a measure of the overall kidney size. The occurrence of IRR is dependent of the papillary morphology, intrapelvic pressure and urine flow. There may be an important relationship between renal ischemia and IRR in producing a 'vicious circle of deleterious effects' which, combined with parenchymal extravasation, may lead to RN. Treatment of VUR includes medical and surgical management. Since renal scarring may occur in infancy, prevention should focus on infants and young children. Infants and young children with severe VUR may have normal urograms. Therefore a MCU should also be performed, preferably with the recommended standardized technique.
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PMID:Vesicoureteral reflux and reflux nephropathy. 388 98


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