Treatment of Renovascular Hypertension

Aurell, Mattias; Jensen, Gert

doi:10.1159/000189574

Cited by 30 publications

(11 citation statements)

References 57 publications

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“…However, available data justify the following recommendations: 1) Refractory hypertension (i.e. persistent blood pressure normalization or reduction with values more responsive to drug treatment [787,791]. persistent blood pressure normalization or reduction with values more responsive to drug treatment [787,791].…”

Section: Renovascular Hypertensionmentioning

confidence: 99%

2007 Guidelines for the Management of Arterial Hypertension

Mancia

Backer

Dominiczak

et al. 2007

Journal of Hypertension

4,843

1,188

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Table 2 Factors influencing prognosis Risk factors Subclinical Organ Damage Systolic and diastolic BP levels Electrocardiographic LVH (Sokolow-Lyon > 38 mm; Cornell > 2440 mm M ms) or: Levels of pulse pressure (in the elderly) Echocardiographic LVH8 (LVMI M ! 125 g/m 2 , W ! 110 g/m 2 ) Age (M > 55 years; W > 65 years) Carotid wall thickening (IMT > 0.9 mm) or plaque Smoking Carotid-femoral pulse wave velocity >12 m/s Dyslipidaemia Ankle/brachial BP index < 0.9 -TC > 5.0 mmol/l (190 mg/dl) or:Slight increase in plasma creatinine:-LDL-C > 3.0 mmol/l (115 mg/dl) or: M: 115-133 mmol/l (1.3-1.5 mg/dl); -HDL-C: M < 1.0 mmol/l (40 mg/dl), W < 1.2 mmol/l (46 mg/dl) or:Low estimated glomerular filtration rate y (< 60 ml/min/1.73 m 2 ) or creatinine clearance^(< 60 ml/min) -TG > 1.7 mmol/l (150 mg/dl) Fasting plasma glucose 5.6-6.9 mmol/L (102-125 mg/dl) Microalbuminuria 30-300 mg/24 h or albumin-creatinine ratio: ! 22 (M); or ! 31(W) mg/g creatinine Abnormal glucose tolerance test Abdominal obesity (Waist circumference > 102 cm (M), > 88 cm (W)) Family history of premature CV disease (M at age < 55 years; W at age < 65 years) Diabetes Mellitus Established CV or renal disease Fasting plasma glucose ! 7.0 mmol/l (126 mg/dl) on repeated measurements, or Cerebrovascular disease: ischaemic stroke; cerebral haemorrhage; transient ischaemic attack Postload plasma glucose > 11.0 mmol/l (198 mg/dl) Heart disease: myocardial infarction; angina; coronary revascularization; heart failure Renal disease: diabetic nephropathy; renal impairment (serum creatinine M > 133, W > 124 mmol/l); proteinuria (> 300 mg/24 h) Peripheral artery disease Advanced retinopathy: haemorrhages or exudates, papilloedema Note: the cluster of three out of 5 risk factors among abdominal obesity, altered fasting plasma glucose, BP > --130/85 mmHg, low HDL-cholesterol and high TG (as defined above) indicates the presence of metabolic syndrome M: men; W: women; CV: cardiovascular disease; IMT: intima-media thickness; BP: blood pressure; TG: triglycerides; C: cholesterol;^Cockroft Gault formula; y MDRD formula; 8Risk maximal for concentric LVH (left ventricular hypertrophy): increased LVMI (left ventricular mass index) with a wall thickness/radius ratio ! 0.42.

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Section: Renovascular Hypertensionmentioning

confidence: 99%

2007 Guidelines for the Management of Arterial Hypertension

Mancia

Backer

Dominiczak

et al. 2007

Journal of Hypertension

4,843

1,188

View full text Add to dashboard Cite

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“…8–10 Arterial hypertension develops from disorders in arterial blood pressure controlling mechanisms and from a disturbed relationship between vasodilative and vasoconstrictive factors. 11 …”

Section: Introductionmentioning

confidence: 99%

Dynamics of calcitonin gene-related peptide-like cells changes in the lungs of two-kidney, one-clip rats

Kasacka

Arciszewska

2012

Eur J Histochem

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Taking into consideration renal hypertension-induced homeostatic disorders and the key role of calcitonin gene-related peptide (CGRP) in many, systemic functions regulating systems, a question arises as to what an extent arterial hypertension affects the morphology and dynamics of pulmonary CGRP-immunopositive cell changes. The aim of the present study was to examine the distribution, morphology and dynamics of changes of CGRP-containing cells in the lungs of rats in the two-kidney, one-clip (2K1C) renovascular hypertension model. The studies were carried out on the lungs of rats after 3, 14, 28, 42, and 91 days long period from the renal artery clipping procedure. In order to identify neuroendocrine cells, immunohistochemical reaction was performed with the use of a specific antibody against CGRP. It was revealed that renovascular hypertension caused changes in the neuroendocrine, CGRP-containing cells in the lungs of rats. The changes, observed in the neuroendocrine cells, depended on time periods from experimentally induced hypertension. The highest intensity of changes in the neuroendocrine cells was observed in the lungs of rats after 14 days from the surgery.

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“…49 Figure 37.16 summarizes 17 reported series assessing technical success and clinical effect of PTRA in patients with RVH due to FMD. 50 Although primary technical success rates for PTRA are high (>90%) for FMD, clinicians need to be aware of the potential for restenosis due to either inadequate initial treatment or recurrent fibrosis. This can be treated by repeated PTRA if needed.…”

Section: Percutaneous Transluminal Renal Angioplasty and Stenting Fibmentioning

confidence: 99%